Multi-omics analysis of pediatric minimally differentiated acute myeloid leukemia reveals RUNX1-driven stemness and chemoresistance.

doi:10.1038/s41375-026-02967-6

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

Multi-omics analysis of pediatric minimally differentiated acute myeloid leukemia reveals RUNX1-driven stemness and chemoresistance.

Leukemia - 1 Jul 2026

Kamitori Tatsuya, Saida Satoshi, Mitani Kazuki, Tsujimoto Shinichi, Goto Hiroaki, Shibata Hirofumi, Akazawa Ryo, Isobe Kiyotaka, Ueno Hiroo, Kakiuchi Nobuyuki, Saito Akiko M, Hiwatari Mitsuteru, Kudo Ko, Hirabayashi Shinsuke, Fukuoka Kohei, Koh Katsuyoshi, Taga Takashi, Kubota Hirohito, Kato Itaru, Umeda Katsutsugu, Adachi Souichi, Kawai Tomoko, Tomizawa Daisuke, Ikeda Junji, Shiba Norio, Hayashi Yasuhide, Ogawa Seishi, Takita Junko

Abstract excerpt

Minimally differentiated acute myeloid leukemia (AML-M0) is a rare and therapeutically challenging subgroup of AML characterized by immature hematopoietic stem cell-like features. To uncover the molecular basis, we conducted a comprehensive multi-omics analysis of 23 pediatric AML-M0 cases and compared them with 1483 leukemia samples. AML-M0 formed a characteristic group that exhibited global DNA hypermethylation...

Read the complete abstract on PubMed

Topics

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

Share to Cell Differentiation

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Core Binding Factor Alpha 2 Subunit

Share to DNA Methylation

Share to Drug Resistance, Neoplasm

Share to Gene Expression Regulation, Leukemic

Share to Leukemia, Myeloid, Acute

Share to Multiomics

Share to Neoplastic Stem Cells

Source

Open in PubMed Open full text

Identifiers

PMID: 42056531
DOI: 10.1038/s41375-026-02967-6
PMCID: PMC13322964

Genes

RUNX1
ETV6
FLT3

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Multi-omics analysis of pediatric minimally differentiated acute myeloid leukemia reveals RUNX1-driven stemness and chemoresistance.PMID 42056531Read ↗

Epigenetic Modifications in Acute Myeloid Leukemia: Prognosis, Treatment, and HeterogeneitySemantic proximity Read ↗

Recent advances in the understanding and treatment of acute myeloid leukemiaSemantic proximity Read ↗

Pediatric non-Down syndrome acute megakaryoblastic leukemia is characterized by distinct genomic subsets with varying outcomes.Semantic proximity Read ↗

Biomarkers and advances in AML-MRC: from bench to bedside.Semantic proximity Read ↗

Uncommon cytogenetic abnormalities identifying high-risk acute myeloid leukemia in children.Semantic proximity Read ↗

The molecular landscape of pediatric acute myeloid leukemia reveals recurrent structural alterations and age-specific mutational interactionsSemantic proximity Read ↗

Insights into the molecular profiles of adult and paediatric acute myeloid leukaemiaSemantic proximity Read ↗

Hematopoietic stem cells acquire survival advantage by loss of RUNX1 methylation identified in familial leukemia.Semantic proximity Read ↗

Longitudinal single-cell profiling of chemotherapy response in acute myeloid leukemiaSemantic proximity Read ↗

Sequence-dependent splicing dysregulation drives therapy resistance in pediatric AML.Semantic proximity Read ↗

RUNX1 mutations in pediatric acute myeloid leukemia are associated with distinct genetic features and an inferior prognosisSemantic proximity Read ↗

Pediatric acute myeloid leukemia: biology and therapeutic implications of genomic variants.Semantic proximity Read ↗

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