2024
Clonal Dissection of MDS and Secondary AML Resolves Shared Splicing Neoantigens and Mechanistic Underpinnings of Hypomethylating Agent Therapeutic Response
Zhang X, Li G, Oliverio A, VanOudenhove J, DeZern A, Ghiaur G, Halene S, Grimes H, Salomonis N. Clonal Dissection of MDS and Secondary AML Resolves Shared Splicing Neoantigens and Mechanistic Underpinnings of Hypomethylating Agent Therapeutic Response. Blood 2024, 144: 1810-1810. DOI: 10.1182/blood-2024-211099.Peer-Reviewed Original ResearchHematopoietic stem cellsHypomethylating agent therapyHypomethylating agentsMyelodysplastic syndromeSecondary AMLBone marrow hematopoietic stem cellsHigh-risk myelodysplastic syndromeQuiescent hematopoietic stem cellsMarrow hematopoietic stem cellsSplicing alterationsPrimary myelodysplastic syndromesMyelodysplastic syndrome patientsGene programHeterogeneous hematological disorderMDS therapyAged bone marrowAssociated with down-regulationHuman hematopoietic progenitorsSingle-cell populationsAssociated with mutationsSurface protein expressionGene expressionCell statesIllumina short readsPrimitive HSCs
2022
Prognostic implications of mono-hit and multi-hit TP53 alterations in patients with acute myeloid leukemia and higher risk myelodysplastic syndromes treated with azacitidine-based therapy
Zeidan A, Bewersdorf J, Hasle V, Shallis R, Thompson E, de Menezes D, Rose S, Boss I, Halene S, Haferlach T, Fox B. Prognostic implications of mono-hit and multi-hit TP53 alterations in patients with acute myeloid leukemia and higher risk myelodysplastic syndromes treated with azacitidine-based therapy. Leukemia 2022, 37: 240-243. PMID: 36437356, DOI: 10.1038/s41375-022-01766-z.Peer-Reviewed Original ResearchConceptsHigh-risk myelodysplastic syndromeRisk myelodysplastic syndromesAcute myeloid leukemiaMyelodysplastic syndromePrognostic implicationsMyeloid leukemiaTP53 alterationsPatientsSyndromeTherapyLeukemiaSelective inhibition of MCL1 overcomes venetoclax resistance in a murine model of myelodysplastic syndromes
Fischer MA, Song Y, Arrate MP, Gbyli R, Villaume MT, Smith BN, Childress MA, Stricker TP, Halene S, Savona MR. Selective inhibition of MCL1 overcomes venetoclax resistance in a murine model of myelodysplastic syndromes. Haematologica 2022, 108: 522-531. PMID: 35979721, PMCID: PMC9890032, DOI: 10.3324/haematol.2022.280631.Peer-Reviewed Original ResearchConceptsB-cell lymphoma 2Acute myeloid leukemiaMyeloid cell leukemia-1Myelodysplastic syndromeMDS subtypesHigh-risk myelodysplastic syndromeMCL1 inhibitionRisk myelodysplastic syndromesAnti-apoptotic protein B-cell lymphoma 2Protein B-cell lymphoma 2Effective clinical therapySelective inhibitorMDS patient samplesAttractive therapeutic opportunityBcl-xLExcess blastsOlder patientsClinical trialsMyeloid leukemiaMurine modelImpressive responseSignificant injuryAnti-apoptotic protein Bcl-xLLeukemia survivalLymphoma 2