Proteomics

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Effect of BET inhibitor, mivebresib, dactolisib or LCL-161 on protein expressions in AML cells with MECOM rearrangement and high expression of EVI1

ABSTRACT: Patient-derived AML194 (acute myeloid leukemia with inv3(q21;q26.2)) cells were treated in duplicate with 0 nM or 500 nM of mivebresib, 500 nM of dual PI3K/mTOR inhibitor dactolisib or 1000 nM of IAP antagonist LCL-161 for 24 hours to determine the global protein expression alterations that correlate with the cell cycle, growth inhibitory and lethal effects of treatment with these small molecules in MECOM-rearranged AML cells with EVI1 overexpression.

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human)

SUBMITTER: Antrix Jain  

LAB HEAD: Dr Kapil Bhalla

PROVIDER: PXD063413 | Pride | 2026-02-16

REPOSITORIES: Pride

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Dataset's files

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Action DRS
53759_1_ECL_1136_hs_TMT10_prof_250ng_F01.pepXML Pepxml
53759_1_ECL_1136_hs_TMT10_prof_250ng_F01.raw Raw
53759_1_ECL_1136_hs_TMT10_prof_250ng_F01.tsv Tabular
53759_1_ECL_1136_hs_TMT10_prof_250ng_F02.pepXML Pepxml
53759_1_ECL_1136_hs_TMT10_prof_250ng_F02.raw Raw
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Publications

MECOM rearrangement in AML involves either inv(3)(q21;q26.2) or t(3;3)(q21;q26.2), where the dislocated GATA2 enhancer drives overexpression of the transcriptional regulator EVI1, causes concomitant GATA2 repression, and promotes AML progression, aggressive phenotype and therapy refractoriness. Treatment with BET protein inhibitor (BETi) induces in vitro and in vivo efficacy in MECOM-r AML cells. Utilizing an unbiased, high-throughput drug screen, focused on mechanistically-annotated drugs, we i  ...[more]

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