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dc.contributor.authorAasebø, Elise
dc.contributor.authorBerven, Frode
dc.contributor.authorHovland, Randi
dc.contributor.authorDoskeland, Stein Ove
dc.contributor.authorBruserud, Øystein
dc.contributor.authorSelheim, Frode
dc.contributor.authorHernandez-Valladares, Maria
dc.date.accessioned2021-05-18T12:18:21Z
dc.date.available2021-05-18T12:18:21Z
dc.date.created2020-11-26T12:40:16Z
dc.date.issued2020
dc.PublishedCancers. 2020, 12 (6), 1-13.
dc.identifier.issn2072-6694
dc.identifier.urihttps://hdl.handle.net/11250/2755484
dc.description.abstractAcute myeloid leukemia (AML) is an aggressive hematological malignancy. Nearly 50% of the patients who receive the most intensive treatment develop chemoresistant leukemia relapse. Although the leukemogenic events leading to relapse seem to differ between patients (i.e., regrowth from a clone detected at first diagnosis, progression from the original leukemic or preleukemic stem cells), a common characteristic of relapsed AML is increased chemoresistance. The aim of the present study was to investigate at the proteomic level whether leukemic cells from relapsed patients present overlapping molecular mechanisms that contribute to this chemoresistance. We used liquid chromatography–tandem mass spectrometry (LC–MS/MS) to compare the proteomic and phosphoproteomic profiles of AML cells derived from seven patients at the time of first diagnosis and at first relapse. At the time of first relapse, AML cells were characterized by increased levels of proteins important for various mitochondrial functions, such as mitochondrial ribosomal subunit proteins (MRPL21, MRPS37) and proteins for RNA processing (DHX37, RNA helicase; RPP40, ribonuclease P component), DNA repair (ERCC3, DNA repair factor IIH helicase; GTF2F1, general transcription factor), and cyclin-dependent kinase (CDK) activity. The levels of several cytoskeletal proteins (MYH14/MYL6/MYL12A, myosin chains; VCL, vinculin) as well as of proteins involved in vesicular trafficking/secretion and cell adhesion (ITGAX, integrin alpha-X; CD36, platelet glycoprotein 4; SLC2A3, solute carrier family 2) were decreased in relapsed cells. Our study introduces new targetable proteins that might direct therapeutic strategies to decrease chemoresistance in relapsed AML.en_US
dc.language.isoengen_US
dc.publisherMDPIen_US
dc.rightsNavngivelse 4.0 Internasjonal*
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/deed.no*
dc.titleThe progression of acute myeloid leukemia from first diagnosis to chemoresistant relapse: A comparison of proteomic and phosphoproteomic profilesen_US
dc.typeJournal articleen_US
dc.typePeer revieweden_US
dc.description.versionpublishedVersionen_US
dc.rights.holderCopyright the authors.en_US
dc.source.articlenumber1466en_US
cristin.ispublishedtrue
cristin.fulltextoriginal
cristin.qualitycode1
dc.identifier.doi10.3390/cancers12061466
dc.identifier.cristin1852822
dc.source.journalCancersen_US
dc.source.4012
dc.source.146
dc.identifier.citationCancers. 2020, 12 (6), 1466.en_US
dc.source.volume12en_US
dc.source.issue6en_US


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Navngivelse 4.0 Internasjonal
Except where otherwise noted, this item's license is described as Navngivelse 4.0 Internasjonal