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.firstpage","553"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Nucleic Acids Research"],["dc.bibliographiccitation.lastpage","564"],["dc.bibliographiccitation.volume","43"],["dc.contributor.author","Sloan, Katherine E."],["dc.contributor.author","Leisegang, Matthias S."],["dc.contributor.author","Doebele, Carmen"],["dc.contributor.author","Ramirez, Ana S."],["dc.contributor.author","Simm, Stefan"],["dc.contributor.author","Safferthal, Charlotta"],["dc.contributor.author","Kretschmer, Jens"],["dc.contributor.author","Schorge, Tobias"],["dc.contributor.author","Markoutsa, Stavroula"],["dc.contributor.author","Haag, Sara"],["dc.contributor.author","Karas, Michael"],["dc.contributor.author","Ebersberger, Ingo"],["dc.contributor.author","Schleiff, Enrico"],["dc.contributor.author","Watkins, Nicholas J."],["dc.contributor.author","Bohnsack, Markus T."],["dc.date.accessioned","2018-11-07T10:03:32Z"],["dc.date.available","2018-11-07T10:03:32Z"],["dc.date.issued","2015"],["dc.description.abstract","Translation fidelity and efficiency require multiple ribosomal (r)RNA modifications that are mostly mediated by small nucleolar (sno)RNPs during ribosome production. Overlapping basepairing of snoRNAs with pre-rRNAs often necessitates sequential and efficient association and dissociation of the snoRNPs, however, how such hierarchy is established has remained unknown so far. Here, we identify several late-acting snoRNAs that bind pre-40S particles in human cells and show that their association and function in pre-40S complexes is regulated by the RNA helicase DDX21. We map DDX21 crosslinking sites on pre-rRNAs and show their overlap with the basepairing sites of the affected snoRNAs. While DDX21 activity is required for recruitment of the late-acting snoRNAs SNORD56 and SNORD68, earlier snoRNAs are not affected by DDX21 depletion. Together, these observations provide an understanding of the timing and ordered hierarchy of snoRNP action in pre-40S maturation and reveal a novel mode of regulation of snoRNP function by an RNA helicase in human cells."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2014"],["dc.identifier.doi","10.1093/nar/gku1291"],["dc.identifier.isi","000350207100052"],["dc.identifier.pmid","25477391"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/11460"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/38490"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation.issn","1362-4962"],["dc.relation.issn","0305-1048"],["dc.rights","CC BY-NC 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc/4.0"],["dc.title","The association of late-acting snoRNPs with human pre-ribosomal complexes requires the RNA helicase DDX21"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.version","published_version"],["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"]]