Döbele, Carmen

[["dc.bibliographiccitation.firstpage","301"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Cancer Cell"],["dc.bibliographiccitation.lastpage","317.e12"],["dc.bibliographiccitation.volume","40"],["dc.contributor.author","Jayavelu, Ashok Kumar"],["dc.contributor.author","Wolf, Sebastian"],["dc.contributor.author","Buettner, Florian"],["dc.contributor.author","Alexe, Gabriela"],["dc.contributor.author","Häupl, Björn"],["dc.contributor.author","Comoglio, Federico"],["dc.contributor.author","Schneider, Constanze"],["dc.contributor.author","Doebele, Carmen"],["dc.contributor.author","Fuhrmann, Dominik C."],["dc.contributor.author","Wagner, Sebastian"],["dc.contributor.author","Oellerich, Thomas"],["dc.date.accessioned","2022-04-01T10:00:59Z"],["dc.date.available","2022-04-01T10:00:59Z"],["dc.date.issued","2022"],["dc.identifier.doi","10.1016/j.ccell.2022.02.006"],["dc.identifier.pii","S1535610822000587"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/105572"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-530"],["dc.relation.issn","1535-6108"],["dc.rights.uri","https://www.elsevier.com/tdm/userlicense/1.0/"],["dc.title","The proteogenomic subtypes of acute myeloid leukemia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","549"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Cancer Cell"],["dc.bibliographiccitation.lastpage","+"],["dc.bibliographiccitation.volume","31"],["dc.contributor.author","Mohr, Sebastian"],["dc.contributor.author","Döbele, Carmen"],["dc.contributor.author","Comoglio, Federico"],["dc.contributor.author","Berg, Tobias"],["dc.contributor.author","Beck, Julia"],["dc.contributor.author","Bohnenberger, Hanibal"],["dc.contributor.author","Alexe, Gabriela"],["dc.contributor.author","Corso, Jasmin"],["dc.contributor.author","Ströbel, Philipp"],["dc.contributor.author","Wachter, Astrid"],["dc.contributor.author","Beißbarth, Tim"],["dc.contributor.author","Schnuetgen, Frank"],["dc.contributor.author","Cremer, Anjali"],["dc.contributor.author","Haetscher, Nadine"],["dc.contributor.author","Goellner, Stefanie"],["dc.contributor.author","Rouhi, Arefeh"],["dc.contributor.author","Palmqvist, Lars"],["dc.contributor.author","Rieger, Michael A."],["dc.contributor.author","Schroeder, Timm"],["dc.contributor.author","Boenig, Halvard"],["dc.contributor.author","Meuller-Tidow, Carsten"],["dc.contributor.author","Kuchenbauer, Florian"],["dc.contributor.author","Schuetz, Ekkehard"],["dc.contributor.author","Green, Anthony R."],["dc.contributor.author","Urlaub, Henning"],["dc.contributor.author","Stegmaier, Kimberly"],["dc.contributor.author","Humphries, R. Keith"],["dc.contributor.author","Serve, Hubert"],["dc.contributor.author","Oellerich, Thomas"],["dc.date.accessioned","2018-11-07T10:25:02Z"],["dc.date.available","2018-11-07T10:25:02Z"],["dc.date.issued","2017"],["dc.description.abstract","The transcription factor Meis1 drives myeloid leukemogenesis in the context of Hox gene overexpression but is currently considered undruggable. We therefore investigated whether myeloid progenitor cells transformed by Hoxa9 and Meis1 become addicted to targetable signaling pathways. A comprehensive (phospho) proteomic analysis revealed that Meis1 increased Syk protein expression and activity. Syk upregulation occurs through a Meis1-dependent feedback loop. By dissecting this loop, we show that Syk is a direct target of miR-146a, whose expression is indirectly regulated by Meis1 through the transcription factor PU. 1. In the context of Hoxa9 overexpression, Syk signaling induces Meis1, recapitulating several leukemogenic features of Hoxa9/Meis1-driven leukemia. Finally, Syk inhibition disrupts the identified regulatory loop, prolonging survival of mice with Hoxa9/Meis1-driven leukemia."],["dc.identifier.doi","10.1016/j.ccell.2017.03.001"],["dc.identifier.isi","000398670600010"],["dc.identifier.pmid","28399410"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14438"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/42772"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Cell Press"],["dc.relation.issn","1878-3686"],["dc.relation.issn","1535-6108"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Hoxa9 and Meis1 Cooperatively Induce Addiction to Syk Signaling by Suppressing miR-146a in Acute Myeloid Leukemia"],["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.journal","Haematologica"],["dc.bibliographiccitation.volume","100"],["dc.contributor.author","Oellerich, Thomas"],["dc.contributor.author","Corso, Jasmin"],["dc.contributor.author","Beck, J."],["dc.contributor.author","Pan, K.-T."],["dc.contributor.author","Döbele, Carmen"],["dc.contributor.author","Wachter, Astrid"],["dc.contributor.author","Lenz, Christof"],["dc.contributor.author","Beißbarth, Tim"],["dc.contributor.author","Schuetz, Eckehardt"],["dc.contributor.author","Tomska, Katarzyna"],["dc.contributor.author","Sellner, L."],["dc.contributor.author","Zenz, Thorsten"],["dc.contributor.author","Serve, Hubert"],["dc.contributor.author","Urlaub, Henning"],["dc.date.accessioned","2018-11-07T09:56:10Z"],["dc.date.available","2018-11-07T09:56:10Z"],["dc.date.issued","2015"],["dc.format.extent","178"],["dc.identifier.isi","000361204901386"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/36907"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Ferrata Storti Foundation"],["dc.publisher.place","Pavia"],["dc.relation.eventlocation","Vienna, AUSTRIA"],["dc.relation.issn","0390-6078"],["dc.title","THE B CELL RECEPTOR SIGNALING OUTPUT IN BURKITT'S LYMPHOMA IS GENOTYPE-SPECIFIC AND IMPACTS SENSITIVITY TOWARDS BCR SIGNALING INHIBITORS"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Blood"],["dc.contributor.author","Wilke, Anne C"],["dc.contributor.author","Doebele, Carmen"],["dc.contributor.author","Zindel, Alena"],["dc.contributor.author","Lee, Kwang Seok"],["dc.contributor.author","Rieke, Sara A."],["dc.contributor.author","Ceribelli, Michele"],["dc.contributor.author","Comoglio, Federico"],["dc.contributor.author","Phelan, James D."],["dc.contributor.author","Wang, James Q"],["dc.contributor.author","Pikman, Yana"],["dc.contributor.author","Oellerich, Thomas"],["dc.date.accessioned","2021-12-01T09:23:09Z"],["dc.date.available","2021-12-01T09:23:09Z"],["dc.date.issued","2021"],["dc.description.abstract","Burkitt lymphoma (BL) is an aggressive lymphoma type that is currently treated by intensive chemoimmunotherapy. Despite the favorable clinical outcome of the majority of BL patients, chemotherapy-related toxicity and disease relapse remain as major clinical challenges, emphasizing the need for innovative therapies. Using genome-scale CRISPR-Cas9 screens, we identified B-cell receptor (BCR) signaling, specific transcriptional regulators and one-carbon metabolism as vulnerabilities in BL. We focused on serine hydroxymethyltransferase 2 (SHMT2), a key enzyme in one-carbon metabolism. Inhibition of SHMT2 by either knockdown or pharmacological compounds induced anti-BL effects in vitro and in vivo. Mechanistically, SHMT2 inhibition led to a significant reduction of intracellular glycine and formate levels, which inhibited the mTOR pathway and thereby triggered autophagic degradation of the oncogenic transcription factor TCF3. As a consequence, this led to a collapse of tonic B-cell receptor signaling, which is controlled by TCF3 and is essential for BL cell survival. In terms of clinical translation, we furthermore identified drugs such as methotrexate that synergized with SHMT inhibitors (SHMT2i). Overall, our study has uncovered the dependency landscape in BL, identified and validated SHMT2 as a drug target and revealed a mechanistic link between SHMT2 and the transcriptional master regulator TCF3, opening up new perspectives for innovative therapies."],["dc.description.abstract","Burkitt lymphoma (BL) is an aggressive lymphoma type that is currently treated by intensive chemoimmunotherapy. Despite the favorable clinical outcome of the majority of BL patients, chemotherapy-related toxicity and disease relapse remain as major clinical challenges, emphasizing the need for innovative therapies. Using genome-scale CRISPR-Cas9 screens, we identified B-cell receptor (BCR) signaling, specific transcriptional regulators and one-carbon metabolism as vulnerabilities in BL. We focused on serine hydroxymethyltransferase 2 (SHMT2), a key enzyme in one-carbon metabolism. Inhibition of SHMT2 by either knockdown or pharmacological compounds induced anti-BL effects in vitro and in vivo. Mechanistically, SHMT2 inhibition led to a significant reduction of intracellular glycine and formate levels, which inhibited the mTOR pathway and thereby triggered autophagic degradation of the oncogenic transcription factor TCF3. As a consequence, this led to a collapse of tonic B-cell receptor signaling, which is controlled by TCF3 and is essential for BL cell survival. In terms of clinical translation, we furthermore identified drugs such as methotrexate that synergized with SHMT inhibitors (SHMT2i). Overall, our study has uncovered the dependency landscape in BL, identified and validated SHMT2 as a drug target and revealed a mechanistic link between SHMT2 and the transcriptional master regulator TCF3, opening up new perspectives for innovative therapies."],["dc.identifier.doi","10.1182/blood.2021012081"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/94576"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-478"],["dc.relation.eissn","1528-0020"],["dc.relation.issn","0006-4971"],["dc.title","SHMT2 inhibition disrupts the TCF3 transcriptional survival program in Burkitt lymphoma"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","23"],["dc.bibliographiccitation.journal","Blood"],["dc.bibliographiccitation.volume","126"],["dc.contributor.author","Doebele, Carmen"],["dc.contributor.author","Kovar, Johannes"],["dc.contributor.author","Yepes, Diego"],["dc.contributor.author","Muench, Silvia"],["dc.contributor.author","Schnuetgen, Frank"],["dc.contributor.author","Bohnenberger, Hanibal"],["dc.contributor.author","Koehler, Anne"],["dc.contributor.author","Urlaub, Henning"],["dc.contributor.author","Serve, Hubert"],["dc.contributor.author","Oellerich, Thomas"],["dc.date.accessioned","2018-11-07T09:47:45Z"],["dc.date.available","2018-11-07T09:47:45Z"],["dc.date.issued","2015"],["dc.identifier.isi","000368020101291"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/35167"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Soc Hematology"],["dc.publisher.place","Washington"],["dc.relation.conference","57th Annual Meeting of the American-Society-of-Hematology"],["dc.relation.eventlocation","Orlando, FL"],["dc.relation.issn","1528-0020"],["dc.relation.issn","0006-4971"],["dc.title","Phosphoproteomic Profiling of the Signaling Output of FLT3-ITD and Its AC220-Resistant Mutants Reveals Profound Signaling Differences and Differential Responsiveness to Inhibition of Downstream Kinases"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Oncology Research and Treatment"],["dc.bibliographiccitation.volume","39"],["dc.contributor.author","Walter, Roland"],["dc.contributor.author","Corso, Jasmin"],["dc.contributor.author","Pan, K.-T"],["dc.contributor.author","Doebele, Carmen"],["dc.contributor.author","Yepes, Diego"],["dc.contributor.author","Sellner, L."],["dc.contributor.author","Tomska, Katarzyna"],["dc.contributor.author","Bohnenberger, H."],["dc.contributor.author","Zenz, Thorsten"],["dc.contributor.author","Urlaub, Henning"],["dc.contributor.author","Serve, Hubert"],["dc.contributor.author","Oellerich, Thomas"],["dc.date.accessioned","2018-11-07T10:07:37Z"],["dc.date.available","2018-11-07T10:07:37Z"],["dc.date.issued","2016"],["dc.format.extent","219"],["dc.identifier.isi","000385691300540"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/39316"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Karger"],["dc.publisher.place","Basel"],["dc.relation.issn","2296-5262"],["dc.relation.issn","2296-5270"],["dc.title","Elucidation of tonic and activated B cell receptor signaling in Burkitt's lymphoma reveals insights into non-oncogene addiction"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","26318"],["dc.bibliographiccitation.issue","42"],["dc.bibliographiccitation.journal","Proceedings of the National Academy of Sciences"],["dc.bibliographiccitation.lastpage","26327"],["dc.bibliographiccitation.volume","117"],["dc.contributor.author","Fish, Kamonwan"],["dc.contributor.author","Comoglio, Federico"],["dc.contributor.author","Shaffer, Arthur L."],["dc.contributor.author","Ji, Yanlong"],["dc.contributor.author","Pan, Kuan-Ting"],["dc.contributor.author","Scheich, Sebastian"],["dc.contributor.author","Oellerich, Angelika"],["dc.contributor.author","Doebele, Carmen"],["dc.contributor.author","Ikeda, Masato"],["dc.contributor.author","Schaller, Samantha J."],["dc.contributor.author","Nguyen, Hang"],["dc.contributor.author","Muppidi, Jagan"],["dc.contributor.author","Wright, George W."],["dc.contributor.author","Urlaub, Henning"],["dc.contributor.author","Serve, Hubert"],["dc.contributor.author","Staudt, Louis M."],["dc.contributor.author","Longnecker, Richard"],["dc.contributor.author","Oellerich, Thomas"],["dc.date.accessioned","2021-04-14T08:31:41Z"],["dc.date.available","2021-04-14T08:31:41Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1073/pnas.2007946117"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/83683"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.eissn","1091-6490"],["dc.relation.issn","0027-8424"],["dc.title","Rewiring of B cell receptor signaling by Epstein–Barr virus LMP2A"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","21"],["dc.bibliographiccitation.journal","Blood"],["dc.bibliographiccitation.volume","124"],["dc.contributor.author","Oellerich, Thomas"],["dc.contributor.author","Mohr, Sebastian"],["dc.contributor.author","Beck, Julia"],["dc.contributor.author","Bohnenberger, Hanibal"],["dc.contributor.author","Doebele, Carmen"],["dc.contributor.author","Corso, Jasmin"],["dc.contributor.author","Bug, Gesine"],["dc.contributor.author","Schuetz, Ekkehard"],["dc.contributor.author","Urlaub, Henning"],["dc.contributor.author","Serve, Hubert"],["dc.date.accessioned","2018-11-07T09:31:26Z"],["dc.date.available","2018-11-07T09:31:26Z"],["dc.date.issued","2014"],["dc.identifier.isi","000349233803024"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/31533"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Soc Hematology"],["dc.publisher.place","Washington"],["dc.relation.conference","56th Annual Meeting of the American-Society-of-Hematology"],["dc.relation.eventlocation","San Francisco, CA"],["dc.relation.issn","1528-0020"],["dc.relation.issn","0006-4971"],["dc.title","Syk and Btk Transduce Survival and Proliferation-Inducing Signals By Activating Distinct Signaling Pathways and Transcriptional Programs in AML Cells"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Cancer Research"],["dc.bibliographiccitation.volume","75"],["dc.contributor.author","Döbele, Carmen"],["dc.contributor.author","Corso, Jasmin"],["dc.contributor.author","Cremer, Anjali"],["dc.contributor.author","Muench, Silvia"],["dc.contributor.author","Beck, Julia"],["dc.contributor.author","Lenz, Christof"],["dc.contributor.author","Bohnenberger, Hanibal"],["dc.contributor.author","Wachter, Astrid"],["dc.contributor.author","Beißbarth, Tim"],["dc.contributor.author","Schuetz, Ekkehard"],["dc.contributor.author","Serve, Hubert"],["dc.contributor.author","Urlaub, Henning"],["dc.contributor.author","Oellerich, Thomas"],["dc.date.accessioned","2018-11-07T09:53:25Z"],["dc.date.available","2018-11-07T09:53:25Z"],["dc.date.issued","2015"],["dc.identifier.doi","10.1158/1538-7445.AM2015-50"],["dc.identifier.isi","000371578500047"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/36326"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Assoc Cancer Research"],["dc.publisher.place","Philadelphia"],["dc.relation.eventlocation","Philadelphia, PA"],["dc.relation.issn","1538-7445"],["dc.relation.issn","0008-5472"],["dc.title","Elucidation of B cell receptor signaling in Burkitt's lymphoma reveals novel signaling nodes with potential therapeutic relevance"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1936"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Blood"],["dc.bibliographiccitation.lastpage","1947"],["dc.bibliographiccitation.volume","125"],["dc.contributor.author","Oellerich, Thomas"],["dc.contributor.author","Mohr, Sebastian"],["dc.contributor.author","Corso, Jasmin"],["dc.contributor.author","Beck, Julia"],["dc.contributor.author","Doebele, Carmen"],["dc.contributor.author","Braun, Helene"],["dc.contributor.author","Cremer, Anjali"],["dc.contributor.author","Muench, Silvia"],["dc.contributor.author","Wicht, Johannes"],["dc.contributor.author","Oellerich, Mark F."],["dc.contributor.author","Bug, Gesine"],["dc.contributor.author","Bohnenberger, Hanibal"],["dc.contributor.author","Perske, Christina"],["dc.contributor.author","Schuetz, Ekkehard"],["dc.contributor.author","Urlaub, Henning"],["dc.contributor.author","Serve, Hubert"],["dc.date.accessioned","2018-11-07T09:59:29Z"],["dc.date.available","2018-11-07T09:59:29Z"],["dc.date.issued","2015"],["dc.description.abstract","Acute myeloid leukemia (AML) is driven by niche-derived and cell-autonomous stimuli. Although many cell-autonomous disease drivers are known, niche-dependent signaling in the context of the genetic disease heterogeneity has been difficult to investigate. Here, we analyzed the role of Bruton tyrosine kinase (BTK) in AML. BTK was frequently expressed, and its inhibition strongly impaired the proliferation and survival of AML cells also in the presence of bone marrow stroma. By interactome analysis, (phospho)proteomics, and transcriptome sequencing, we characterized BTK signaling networks. We show that BTK-dependent signaling is highly context dependent. In Fms-like tyrosine kinase 3 internal tandem duplication (FLT3-ITD)-positive AML, BTK mediates FLT3-ITD-dependent Myc and STAT5 activation, and combined targeting of FLT3-ITD and BTK showed additive effects. In Fms-like tyrosine kinase 3 internal tandem duplication (FLT3-ITD)-negative AML, BTK couples Toll-like receptor 9 (TLR9) activation to nuclear factor kappa B and STAT5. Both BTK-dependent transcriptional programs were relevant for cell cycle progression and apoptosis regulation. Thus, we identify context-dependent oncogenic driver events that may guide subtype-specific treatment strategies and, for the first time, point to a role of TLR9 in AML. Clinical evaluation of BTK inhibitors in AML seems warranted."],["dc.identifier.doi","10.1182/blood-2014-06-585216"],["dc.identifier.isi","000354623700017"],["dc.identifier.pmid","25605370"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/37600"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Soc Hematology"],["dc.relation.issn","1528-0020"],["dc.relation.issn","0006-4971"],["dc.title","FLT3-ITD and TLR9 use Bruton tyrosine kinase to activate distinct transcriptional programs mediating AML cell survival and proliferation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]