Evidence map›Paper›PMID 40166939›Full record

ArticleThe Journal of clinical investigation2025

HoxBlinc: a key driver of chromatin dynamics in NUP98 fusion-driven leukemia.

Jian Xu, Wei Du

Abstract read
In one paragraph

Article in The Journal of clinical investigation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. Article
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

2 authors.

Jian XuDivision of Hematology and Oncology, University of Pittsburgh School of Medicine, Pittsburgh, Philadelphia, USA.
Wei DuDivision of Hematology and Oncology, University of Pittsburgh School of Medicine, Pittsburgh, Philadelphia, USA.

Funding

Role of LAM-specific TREM1 in leukemogenesisR01CA285400 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Wei Du · 2024 to 2026
$2.6M
A novel immunometabolism-regulatory axis in inflammatory hematopoiesisR01HL151390 · NHLBI · WEST VIRGINIA UNIVERSITY · PI DU, WEI · 2020 to 2023
$1.5M
A beneficial persistent DNA damage-induced immune response in agingR56HL169348 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI DU, WEI · 2024 to 2024
$710k
NCI NIH HHS R01 CA285400NHLBI NIH HHS R01 HL151390NHLBI NIH HHS R56 HL169348
6 · The paper itself

Abstract

Nucleoporin 98 (NUP98) fusion oncogenes are known to promote aggressive pediatric leukemia by disrupting chromatin structure and modulating the expression of homeobox (HOX) genes, yet the precise molecular events are unclear. In this issue of the JCI, K. Hamamoto et al. explore the mechanistic underpinnings of NUP98 fusion-driven pediatric leukemia, with a focus on aberrant activation of the Hoxb-associated long, noncoding RNA (lncRNA) HoxBlinc. The authors provide compelling evidence that HoxBlinc plays a central role in the oncogenic transformation associated with NUP98 fusion protein. The study underscores a CTCF-independent role of HoxBlinc in the regulation of topologically associated domains (TADs) and chromatin accessibility, which has not been fully appreciated in previous research on the NUP98 fusion oncogenes. The discovery of HoxBlinc lncRNA as a downstream regulator of NUP98 fusion oncoproteins offers a potential target for therapeutic intervention in pediatric leukemia.

Indexed as

ChromatinLeukemiaNuclear Pore Complex ProteinsOncogene Proteins, FusionRNA, Long NoncodingRNA, NeoplasmAnimalsHomeodomain ProteinsHumansChromatinHomeodomain Proteinsnuclear pore complex protein 98Nuclear Pore Complex ProteinsNup98 protein, humanOncogene Proteins, FusionRNA, Long NoncodingRNA, Neoplasm

Identifiers

PMID40166939
PMCPMC11957688

What Socratic holds

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LicenceCC BY
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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 Socratic graph.