Proteomics

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Effect of CDK7 inhibitor, FHD-286, SNDX-50469, or Tasquinimod on protein expression alterations in patient-derived secondary AML or de novo MLL1-rearranged AML cells


ABSTRACT: Patient-derived secondary AML cells were treated with 100 nM of SY-5609 for 24 hours, 100 nM of FHD-286 for 48 hours, or 20 µM of Tasquinimod for 48 hours to determine the global protein expression alterations that correlate with the cell cycle, growth inhibitory and lethal effects of treatment with a CDK7 inhibitor, chromatin remodeling inhibitor, or S100A8/S100A9 inhibitor or in secondary AML cells. Patient-derived de novo AML cells with MLL1 rearrangement and Menin T349M mutation were treated with 100 nM of FHD-286 or 500 nM SNDX-50469 for 48 hours to determine the global protein expression alterations that correlate with the cell cycle, growth inhibitory and/or lethal effects of treatment with a chromatin remodeling inhibitor, FHD-286, or a Menin inhibitor SNDX-50469 in MLL1 rearranged AML cells

INSTRUMENT(S): Orbitrap Exploris 480

ORGANISM(S): Homo Sapiens (human)

SUBMITTER: Antrix Jain  

LAB HEAD: Kapil N. Bhalla

PROVIDER: PXD053548 | Pride | 2025-04-28

REPOSITORIES: Pride

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Publications


<h4>Abstract</h4>Rising blast percentage or secondary acute myeloid leukemia (sAML) transformation in myeloproliferative neoplasms (MPNs) leads to JAK1/2 inhibitor (JAKi) therapy resistance and poor survival. Here, we demonstrate that treatment with the CDK7 inhibitor (CDK7i) SY-5609 depletes phenotypically characterized post-MPN sAML stem/progenitor cells. In cultured post-MPN sAML SET2, HEL and patient-derived (PD) post-MPN sAML cells, SY-5609 treatment inhibited growth and induced lethality w  ...[more]

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