Combining menin and MEK inhibition to target poor prognosis KMT2A-rearranged RAS pathway-mutant acute myeloid leukemia.

doi:10.1182/bloodadvances.2025016208

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Community

Back to search

Article

Combining menin and MEK inhibition to target poor prognosis KMT2A-rearranged RAS pathway-mutant acute myeloid leukemia.

Blood advances - 14 Jul 2026

Scheidegger Nastassja, Schneider Constanze, Alexe Gabriela, Wang Yi-Cheng, Alonzo Todd A, Basanthakumar Allen, Bourgeois Wallace A, Dudkiewicz-Garbicz Julia, Khalid Delan, Merickel Lucy A, Perry Jennifer A, Ries Rhonda E, Salhotra Silvi, Taillon Audrey, Gamis Alan, Aplenc Richard, Harris Marian H, Wunderlich Mark, Armstrong Scott A, Pollard Jessica A, Meshinchi Soheil, Pikman Yana, Stegmaier Kimberly

Abstract excerpt

ABSTRACT: KMT2A-rearranged (KMT2A-r) acute leukemias are especially prevalent in the pediatric population. KMT2A-fusion proteins drive leukemogenic gene expression through an interaction with a chromatin complex that includes the scaffold protein menin, giving rise to aggressive acute leukemias. RAS pathway mutations are also common in pediatric leukemia. In a cohort of 1750 patients enrolled on Children's...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Benzimidazoles

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Gene Rearrangement

Share to Histone-Lysine N-Methyltransferase

Share to Leukemia, Myeloid, Acute

Share to Myeloid-Lymphoid Leukemia Protein

Share to Protein Kinase Inhibitors

Share to Proto-Oncogene Proteins

Share to Xenograft Model Antitumor Assays

Source

Open in PubMed Open full text

Identifiers

PMID: 42085603
DOI: 10.1182/bloodadvances.2025016208
PMCID: PMC13334795

Genes

KMT2A

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Combining menin and MEK inhibition to target poor prognosis KMT2A-rearranged RAS pathway-mutant acute myeloid leukemia.PMID 42085603Read ↗

Combination Strategies with Menin Inhibitors for Acute LeukemiaSemantic proximity Read ↗

Menin inhibitors in KMT2A-rearranged leukemia: Mechanistic insights, clinical trial progress, and potential of combination therapiesSemantic proximity Read ↗

Menin inhibitors in KMT2A-rearranged and NPM1-mutated acute leukemia: A scoping review of safety and efficacySemantic proximity Read ↗

Menin Inhibitors: A New Era of Targeted Therapies in Acute Myeloid Leukemia.Semantic proximity Read ↗

Distinct Responses to Menin Inhibition and Synergy with DOT1L Inhibition in KMT2A-Rearranged Acute Lymphoblastic and Myeloid Leukemia.Semantic proximity Read ↗

Revumenib for patients with acute leukemia: a new tool for differentiation therapySemantic proximity Read ↗

Menin inhibitors in the treatment of acute myeloid leukemiaSemantic proximity Read ↗

Acute Myeloid Leukemias with Alterations of Lysine Methyltransferase 2A (KMT2A): Recent Therapeutic DevelopmentsSemantic proximity Read ↗

Targeting the Menin-KMT2A Axis in Acute Leukemia: From Epigenetic Dependency to Clinical Translation.Semantic proximity Read ↗

Small Molecule Menin Inhibitors: Novel Therapeutic Agents Targeting Acute Myeloid Leukemia with KMT2A Rearrangement or NPM1 MutationSemantic proximity Read ↗

Emerging drug profile: menin inhibitors in NPM1-mutated and KM2A-rearranged acute myeloid leukemia.Semantic proximity Read ↗

Preclinical efficacy of the potent, selective menin-KMT2A inhibitor JNJ-75276617 (bleximenib) in KMT2A- and NPM1-altered leukemiasSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.