Evidence map›Paper›PMID 40334081›Full record

ArticleBlood advances2025

Clec12a is required for the pathogenesis of NUP98::NSD1 AML.

Sagarajit Mohanty, Fiorella Charles Cano, Razif Gabdoulline, Courteney K Lai, Basem Othman, Harish Sudarsanam, Thomas Eder, Florian Grebien, Daniel B Lipka, Reinhard Henschler and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Blood advances, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Review
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

11 authors.

Sagarajit MohantyDepartment of Hematology, Hemostasis, Oncology, and Stem Cell Transplantation, Hannover Medical School, Hannover, Germany.ORCID 0000-0001-7935-7798
Fiorella Charles CanoDepartment of Hematology, Hemostasis, Oncology, and Stem Cell Transplantation, Hannover Medical School, Hannover, Germany.ORCID 0009-0006-3941-7497
Razif GabdoullineDepartment of Hematology, Hemostasis, Oncology, and Stem Cell Transplantation, Hannover Medical School, Hannover, Germany.
Courteney K LaiDepartment of Hematology, Hemostasis, Oncology, and Stem Cell Transplantation, Hannover Medical School, Hannover, Germany.
Basem OthmanDepartment of Hematology, Hemostasis, Oncology, and Stem Cell Transplantation, Hannover Medical School, Hannover, Germany.
Harish SudarsanamInstitute of Transfusion Medicine, University Hospital Leipzig, Leipzig, Germany.
Thomas EderCentre for Biological Sciences, University of Veterinary Medicine Vienna, Vienna, Austria.
Florian GrebienCentre for Biological Sciences, University of Veterinary Medicine Vienna, Vienna, Austria.ORCID 0000-0003-4289-2281
Daniel B LipkaSection of Translational Cancer Epigenomics, Department of Translational Medical Oncology, German Cancer Research Center and National Center for Tumor Diseases, Heidelberg, Germany.ORCID 0000-0001-5081-7869
Reinhard HenschlerInstitute of Transfusion Medicine, University Hospital Leipzig, Leipzig, Germany.
Michael HeuserDepartment of Hematology, Hemostasis, Oncology, and Stem Cell Transplantation, Hannover Medical School, Hannover, Germany.ORCID 0000-0001-5318-9044

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI SELWYN M VICKERS · 1985 to 2026
$347.4M
NCI NIH HHS P30 CA008748
6 · The paper itself

Abstract

abstractNUP98::NSD1 is one of the most recurring nucleoporin 98 (NUP98) fusions in acute myeloid leukemia (AML). NUP98::NSD1 positive AML is often associated with adverse outcomes and poor response to conventional treatments. However, limited studies have been done to identify new potential targets to develop better treatment approaches. The C-type lectin domain family 12 member A (CLEC12A) is a cell surface receptor that is differentially expressed in leukemic stem cells compared with healthy hematopoietic stem cells. We found a strong CLEC12A overexpression in both NUP98::NSD1 patients and murine AML cells transformed with the NUP98::NSD1 fusion oncogene. To understand the role of Clec12a in NUP98::NSD1 AML, we depleted Clec12a expression in NUP98::NSD1+NRASG12D-immortalized cells using the CRISPR/Cas9 approach. NUP98::NSD1+NRASG12D/Clec12a knockout cells had higher apoptosis levels and lower colony numbers in vitro compared with NUP98::NSD1+NRASG12D/Clec12a wild-type cells. Importantly, the deletion of Clec12a significantly reduced leukemic engraftment and prolonged survival of the NUP98::NSD1+NRASG12D murine model. Our data suggest to further explore CLEC12A as a potential target for the treatment of NUP98::NSD1 AML.

Indexed as

Lectins, C-TypeLeukemia, Myeloid, AcuteNuclear Pore Complex ProteinsReceptors, MitogenAnimalsCell Line, TumorGene Expression Regulation, LeukemicHumansMiceOncogene Proteins, FusionCLEC12A protein, humanLectins, C-TypeNuclear Pore Complex ProteinsNup98 protein, humanOncogene Proteins, FusionReceptors, Mitogen

Identifiers

PMID40334081
PMCPMC12332935

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LicenceCC BY-NC-ND
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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.