Evidence map›Paper›PMID 41358901›Full record

ReviewInternational journal of cancer2026

The hidden regulators: Non-coding RNAs in KMT2A-rearranged acute lymphoblastic leukemia.

Maria Augusta Poersch, Ana Carolina Rodrigues, Priscila Elias Ferreira Stricker, Alexandre Luiz Korte Azevedo, Daniel Pacheco Bruschi, Jaqueline Carvalho de Oliveira

Abstract readReview
In one paragraph

Review in International journal of cancer, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

6 authors.

Maria Augusta PoerschGenetics Post-Graduation Program, Genetics Department, Federal University of Parana, Curitiba, Parana, Brazil.ORCID https://orcid.org/0000-0003-4922-3427
Ana Carolina RodriguesGenetics Post-Graduation Program, Genetics Department, Federal University of Parana, Curitiba, Parana, Brazil.
Priscila Elias Ferreira StrickerGenetics Post-Graduation Program, Genetics Department, Federal University of Parana, Curitiba, Parana, Brazil.
Alexandre Luiz Korte AzevedoGenetics Post-Graduation Program, Genetics Department, Federal University of Parana, Curitiba, Parana, Brazil.
Daniel Pacheco BruschiGenetics Post-Graduation Program, Genetics Department, Federal University of Parana, Curitiba, Parana, Brazil.
Jaqueline Carvalho de OliveiraGenetics Post-Graduation Program, Genetics Department, Federal University of Parana, Curitiba, Parana, Brazil.ORCID https://orcid.org/0000-0002-5314-3107

Funding

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior 001
6 · The paper itself

Abstract

Acute lymphoblastic leukemia (ALL) driven by KMT2A rearrangements (KMT2A-r) is an aggressive hematologic malignancy with poor prognosis and a high incidence in infants. While KMT2A fusion proteins drive leukemogenesis through transcriptional dysregulation, recent discoveries have highlighted the pivotal role of non-coding RNAs (ncRNAs) in shaping the molecular and epigenetic landscape of this disease. These key regulators of gene expression influence chromatin dynamics, transcriptional activation, and post-transcriptional control. Circular RNAs (circRNAs) contribute to genome instability and facilitate chromosomal translocations, while some fusion-derived circRNAs (f-circRNAs) sustain oncogenic signaling and promote chemoresistance. Long non-coding RNAs (lncRNAs) orchestrate transcriptional programs that maintain leukemic stem cell properties and reinforce aberrant self-renewal pathways. MicroRNAs (miRNAs) modulate critical oncogenic networks by regulating KMT2A fusion transcripts and downstream effectors, thereby impacting drug resistance, apoptosis, and proliferation. Meanwhile, enhancer RNAs (eRNAs) fine-tune transcriptional activity and epigenetic regulation, influencing KMT2A target gene expression and chromatin accessibility. Collectively, these ncRNAs integrate into the complex regulatory circuits of KMT2A-r ALL, revealing their potential as biomarkers for disease classification, risk stratification, and treatment response prediction. Understanding their interplay with KMT2A fusion proteins not only provides new insights into leukemogenesis but also highlights promising opportunities for therapeutic intervention and precision medicine in this high-risk leukemia subtype.

Indexed as

Histone-Lysine N-MethyltransferaseMyeloid-Lymphoid Leukemia ProteinPrecursor Cell Lymphoblastic Leukemia-LymphomaRNA, UntranslatedAnimalsEpigenesis, GeneticGene Expression Regulation, LeukemicGene RearrangementHumansMicroRNAsOncogene Proteins, FusionRNA, CircularRNA, Long NoncodingHistone-Lysine N-MethyltransferaseKMT2A protein, humanMicroRNAsMyeloid-Lymphoid Leukemia ProteinOncogene Proteins, FusionRNA, CircularRNA, Long NoncodingRNA, Untranslatedacute lymphoblastic leukemiaKMT2A rearrangementmixed lineage leukemianon‐coding RNAs

Identifiers

PMID41358901
PMCPMC12922646

What Socratic holds

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Registered trials

None linked

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.