Dynamic genetic and nongenetic RAS-pathway activation drives resistance to FLT3 and BCL2 inhibitor therapy.

doi:10.1182/blood.2025032466

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Article

Dynamic genetic and nongenetic RAS-pathway activation drives resistance to FLT3 and BCL2 inhibitor therapy.

Blood - 17 Sept 2026

Kennedy Vanessa E, Peretz Cheryl A C, Walia Anushka, Chyla Brenda, Sun Yan, Hill Jason, Tran Elaine, Koh Andrew D, Ferng Timothy, Pintar Samantha, Jones Matthew F, Popescu Bogdan, Lomeli Isabelle, Chehab Farid, Murad Natalia, John August, Roy Ritu, Olshen Adam, Berryhill Christine A, Davis Christopher, Angus Steven P, Rivera Jose M, Meshulam Alicia, Stieglitz Elliot, Joshi Sunil, Traer Elie, Dail Monique, Hamidi Habib, Altman Jessica K, Daver Naval, Levis Mark, McCloskey James, Perl Alexander E, Smith Catherine C

Abstract excerpt

ABSTRACT: Bulk sequencing of relapsed tumors reveals mutations associated with resistance to cancer therapy but is insufficient to fully assess all causes of relapse. Because of inherent tumor heterogeneity, on-treatment tumor evolution may select genetically distinct clones or shifts in malignant transcriptional states not resolvable by bulk sequencing. We performed multiomic single-cell DNA/protein and...

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Topics

Humans
Aniline Compounds
Bridged Bicyclo Compounds, Heterocyclic

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Drug Resistance, Neoplasm

fms-Like Tyrosine Kinase 3

Leukemia, Myeloid, Acute

Mutation

Protein Kinase Inhibitors

Proto-Oncogene Proteins c-bcl-2

Pyrazines

ras Proteins

Signal Transduction

Sulfonamides

Source

Open in PubMed Open full text

Identifiers

PMID: 42224378
DOI: 10.1182/blood.2025032466
PMCID: PMC13249044

Genes

FLT3
BCL2

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 22 Oct 2026.

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