Evidence map›Paper›PMID 39607901›Full record

ReviewStem cells translational medicine2025

Targeting chromatin modifying complexes in acute myeloid leukemia.

Alexandra Schurer, Shira G Glushakow-Smith, Kira Gritsman

Abstract readReview
In one paragraph

Review in Stem cells translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

15 citing papers in PubMed.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors.

Alexandra SchurerDepartment of Cell Biology, Albert Einstein College of Medicine, Bronx, NY 10461, United States.
Shira G Glushakow-SmithDepartment of Cell Biology, Albert Einstein College of Medicine, Bronx, NY 10461, United States.
Kira GritsmanDepartment of Cell Biology, Albert Einstein College of Medicine, Bronx, NY 10461, United States.ORCID 0000-0002-1367-1167

Funding

MEDICAL SCIENTIST TRAINING PROGRAMT32GM007288 · NIGMS · YESHIVA UNIVERSITY · PI AKABAS, MYLES H. · 1985 to 2022
$35.6M
Medical Scientist Training ProgramT32GM149364 · NIGMS · ALBERT EINSTEIN COLLEGE OF MEDICINE · PI Myles H. Akabas · 2023 to 2026
$7.5M
PI3 Kinase Inactivation in Myelodysplastic SyndromeR01DK130895 · NIDDK · ALBERT EINSTEIN COLLEGE OF MEDICINE · PI GRITSMAN, KIRA · 2022 to 2025
$2.2M
PI3K Isoform Dependence in Adult Hematopoiesis and Myeloid LeukemiaR01CA196973 · NCI · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI GRITSMAN, KIRA · 2016 to 2020
$2.0M
NRSA Training CoreTL1TR002557 · NCATS · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI MARANTZ, PAUL R · 2018 to 2022
$1.0M
American Cancer Society RSG-19-130-01-DDCEclipse Training #TL1 TR002557National Institutes of Health Medical Scientist Training Program #T32GM007288NCATS NIH HHS TL1 TR002557NCI NIH HHS R01 CA196973NIDDK NIH HHS R01 DK130895NIGMS NIH HHS T32 GM007288NIGMS NIH HHS T32 GM149364NIH HHSNIH HHS R01CA196973Peer Reviewed Cancer Research Program CA200503
6 · The paper itself

Abstract

Acute myeloid leukemia (AML) is a devastating hematologic malignancy with high rates of relapse, which can, in part, be attributed to the dysregulation of chromatin modifications. These epigenetic modifications can affect the capacity of hematopoietic cells to self-renew or differentiate, which can lead to transformation. Aberrant histone modifications contribute to the derepression of self-renewal genes such as HOXA/B and MEIS1 in committed hematopoietic progenitors, which is considered a key mechanism of leukemogenesis in MLL-rearranged (MLL-r) and NPM1-mutated AML. As regulators of some of the key histone modifications in this disease, the menin-KMT2A and polycomb repressive (PRC1/2) complexes have been identified as promising targets for the treatment of AML. This review explores recent discoveries of how leukemic cells hijack these complexes and their interactions with other chromatin regulators to promote disease progression. We also discuss inhibitors targeting these complexes that have demonstrated therapeutic efficacy in preclinical and clinical studies and propose novel therapeutic combinations targeting the KMT2A and PRC1/2 broader interacting networks to overcome issues of resistance to existing monotherapies.

Indexed as

ChromatinLeukemia, Myeloid, AcuteAnimalsEpigenesis, GeneticHistone-Lysine N-MethyltransferaseHumansMyeloid-Lymphoid Leukemia ProteinNucleophosminChromatinHistone-Lysine N-MethyltransferaseKMT2A protein, humanMyeloid-Lymphoid Leukemia ProteinNPM1 protein, humanNucleophosminacute myeloid leukemiachromatinhistonesHOXA/BKMT2AKMT2A-rearrangementMEIS1menin inhibitionNPM1cPRC1PRC2

Identifiers

PMID39607901
PMCPMC11878770

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.