<HashMap><database>biostudies-literature</database><scores/><additional><submitter>van Dijk AD</submitter><funding>NCI</funding><funding>NIH COG</funding><funding>Junior Scientific Masterclass (Groningen, The Netherlands)</funding><funding>NCI NIH HHS</funding><pagination>1448</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11048007</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>16(8)</volume><pubmed_abstract>The addition of the proteasome inhibitor bortezomib to standard chemotherapy did not improve survival in pediatric acute myeloid leukemia (AML) when all patients were analyzed as a group in the Children's Oncology Group phase 3 trial AAML1031 (NCT01371981). Proteasome inhibition influences the chromatin landscape and proteostasis, and we hypothesized that baseline proteomic analysis of histone- and chromatin-modifying enzymes (HMEs) would identify AML subgroups that benefitted from bortezomib addition. A proteomic profile of 483 patients treated with AAML1031 chemotherapy was generated using a reverse-phase protein array. A relatively high expression of 16 HME was associated with lower EFS and higher 3-year relapse risk after AML standard treatment compared to low expressions (52% vs. 29%,</pubmed_abstract><journal>Cancers</journal><pubmed_title>Chromatin Profiles Are Prognostic of Clinical Response to Bortezomib-Containing Chemotherapy in Pediatric Acute Myeloid Leukemia: Results from the COG AAML1031 Trial.</pubmed_title><pmcid>PMC11048007</pmcid><funding_grant_id>U10 CA180886</funding_grant_id><funding_grant_id>U10 CA98543</funding_grant_id><funding_grant_id>R01-CA164024</funding_grant_id><funding_grant_id>U24 CA196173</funding_grant_id><funding_grant_id>U10 CA180899</funding_grant_id><funding_grant_id>U10 CA98413</funding_grant_id><pubmed_authors>van Dijk AD</pubmed_authors><pubmed_authors>Leonti AR</pubmed_authors><pubmed_authors>Meshinchi S</pubmed_authors><pubmed_authors>Hubner SE</pubmed_authors><pubmed_authors>de Bont ESJM</pubmed_authors><pubmed_authors>Go RL</pubmed_authors><pubmed_authors>Gerbing RB</pubmed_authors><pubmed_authors>Qiu Y</pubmed_authors><pubmed_authors>Kornblau SM</pubmed_authors><pubmed_authors>Gamis AS</pubmed_authors><pubmed_authors>Horton TM</pubmed_authors><pubmed_authors>Aplenc R</pubmed_authors><pubmed_authors>Hoff FW</pubmed_authors><pubmed_authors>Alonzo TA</pubmed_authors><pubmed_authors>Ruvolo VR</pubmed_authors><pubmed_authors>Kolb EA</pubmed_authors></additional><is_claimable>false</is_claimable><name>Chromatin Profiles Are Prognostic of Clinical Response to Bortezomib-Containing Chemotherapy in Pediatric Acute Myeloid Leukemia: Results from the COG AAML1031 Trial.</name><description>The addition of the proteasome inhibitor bortezomib to standard chemotherapy did not improve survival in pediatric acute myeloid leukemia (AML) when all patients were analyzed as a group in the Children's Oncology Group phase 3 trial AAML1031 (NCT01371981). Proteasome inhibition influences the chromatin landscape and proteostasis, and we hypothesized that baseline proteomic analysis of histone- and chromatin-modifying enzymes (HMEs) would identify AML subgroups that benefitted from bortezomib addition. A proteomic profile of 483 patients treated with AAML1031 chemotherapy was generated using a reverse-phase protein array. A relatively high expression of 16 HME was associated with lower EFS and higher 3-year relapse risk after AML standard treatment compared to low expressions (52% vs. 29%,</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Apr</publication><modification>2026-04-08T19:52:15.017Z</modification><creation>2026-04-08T14:32:43.348Z</creation></dates><accession>S-EPMC11048007</accession><cross_references><pubmed>38672531</pubmed><doi>10.3390/cancers16081448</doi></cross_references></HashMap>