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  The proteogenomic subtypes of acute myeloid leukemia

Jayavelu, A. K., Wolf, S., Buettner, F., Alexe, G., Häupl, B., Comoglio, F., et al. (2022). The proteogenomic subtypes of acute myeloid leukemia. Cancer Cell, 40(3), 301-317.e12. doi:10.1016/j.ccell.2022.02.006.

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Datensatz-Permalink: https://hdl.handle.net/21.11116/0000-000B-2977-2 Versions-Permalink: https://hdl.handle.net/21.11116/0000-000B-50CC-5
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Jayavelu, Ashok Kumar, Autor
Wolf, Sebastian, Autor
Buettner, Florian, Autor
Alexe, Gabriela, Autor
Häupl, Björn, Autor
Comoglio, Federico, Autor
Schneider, Constanze, Autor
Doebele, Carmen, Autor
Fuhrmann, Dominik C., Autor
Wagner, Sebastian, Autor
Donato, Elisa, Autor
Andresen, Carolin, Autor
Wilke, Anne C., Autor
Zindel, Alena, Autor
Jahn, Dominique, Autor
Splettstoesser, Bianca, Autor
Plessmann, U.1, Autor           
Münch, Silvia, Autor
Abou-El-Ardat, Khali, Autor
Makowka, Philipp, Autor
Acker, Fabian, AutorEnssle, Julius C., AutorCremer, Anjali, AutorSchnütgen, Frank, AutorKurrle, Nina, AutorChapuy, Björn, AutorLöber, Jens, AutorHartmann, Sylvia, AutorWild, Peter J., AutorWittig, Ilka, AutorHübschmann, Daniel, AutorKaderali, Lars, AutorCox, Jürgen, AutorBrüne, Bernhard, AutorRöllig, Christoph, AutorThiede, Christian, AutorSteffen, Björn, AutorBornhäuser, Martin, AutorTrumpp, Andreas, AutorUrlaub, Henning1, Autor           Stegmaier, Kimberly, AutorServe, Hubert, AutorMann, Matthias, AutorOellerich, Thomas, Autor mehr..
Affiliations:
1Research Group of Bioanalytical Mass Spectrometry, Max Planck Institute for Multidisciplinary Sciences, Max Planck Society, ou_3350290              

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 Zusammenfassung: Acute myeloid leukemia (AML) is an aggressive blood cancer with a poor prognosis. We report a comprehensive proteogenomic analysis of bone marrow biopsies from 252 uniformly treated AML patients to elucidate the molecular pathophysiology of AML in order to inform future diagnostic and therapeutic approaches. In addition to in-depth quantitative proteomics, our analysis includes cytogenetic profiling and DNA/RNA sequencing. We identify five proteomic AML subtypes, each reflecting specific biological features spanning genomic boundaries. Two of these proteomic subtypes correlate with patient outcome, but none is exclusively associated with specific genomic aberrations. Remarkably, one subtype (Mito-AML), which is captured only in the proteome, is characterized by high expression of mitochondrial proteins and confers poor outcome, with reduced remission rate and shorter overall survival on treatment with intensive induction chemotherapy. Functional analyses reveal that Mito-AML is metabolically wired toward stronger complex I-dependent respiration and is more responsive to treatment with the BCL2 inhibitor venetoclax.

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Sprache(n): eng - English
 Datum: 2022
 Publikationsstatus: Erschienen
 Seiten: -
 Ort, Verlag, Ausgabe: -
 Inhaltsverzeichnis: -
 Art der Begutachtung: Expertenbegutachtung
 Identifikatoren: DOI: 10.1016/j.ccell.2022.02.006
 Art des Abschluß: -

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Projektname : We thank H. Lang, S. Mohr, and D. Yepes from the Oellerich laboratory and M. Sohn from the Trumpp laboratory for their technical support. We thank all the members of Proteomics and Signal Transduction Department at the Max Planck Institute for Biochemistry, particularly I. Paron, C. Deiml, J. Müller, G. Sowa, N. Nagaraj, and F. Meier for their technical assistance. We thank the staff of the University Cancer Center (UCT) and the Study Alliance Leukemia (SAL) biobanks for the close collaboration, particularly K. Götze, S. Jordan, M. Berger, and H. Altmann. Genomic sequencing was in parts done by MLL Dx, Munich and we thank particularly T. Haferlach, M. Meggendorfer and N. Nadarajah for expert technical assistance. A.K.J., B.Splettstoesser, and M.M. were supported by the Max Planck Society for the Advancement of Science and by the German Research Foundation (DFG/Gottfried Wilhelm Leibniz Prize). T.O. was supported by the German Research Foundation. S.Wolf was supported by the Else Kröner-Fresenius-Stiftung and the Mildred-Scheel-Nachwuchszentrum (MSNZ, German Cancer Aid). K.S. was supported by NIH R35 CA210030 and NIH P50 CA206963. This work was supported by SPP2036, FOR2674, and SFB873 funded by the Deutsche Forschungsgemeinschaft (DFG); the DKTK joint funding project “RiskY-AML”; and the Dietmar Hopp Foundation (all to A.T.). The graphical abstract was created by Dorotea Fracchiolla, Art&Science.
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Quelle 1

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Titel: Cancer Cell
  Andere : Cancer Cell
Genre der Quelle: Zeitschrift
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Ort, Verlag, Ausgabe: Cambridge, Mass. : Cell Press
Seiten: - Band / Heft: 40 (3) Artikelnummer: - Start- / Endseite: 301 - 317.e12 Identifikator: ISSN: 1535-6108
CoNE: https://pure.mpg.de/cone/journals/resource/111025129473004