ArticleContemporary oncology (Poznan, Poland)2025
Regulation of long non-coding RNA NEAT1 by isoforms of transcription factor C/EBPα in acute myeloid leukemia.
Article in Contemporary oncology (Poznan, Poland), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Acute myeloid leukemia (AML) is a biologically heterogeneous, malignant disease of the hema-topoietic system. In ~10% of AML cases, the full-length isoform (p42) of the transcription factor CCAAT/enhancer binding protein alpha (C/EBPα), an essential regulator of granulopoiesis, is mutated. N-terminal mutations shift expression towards the truncated C/EBPα isoform (p30), promoting proliferation of leukaemic blasts. The self-renewal ability of AML cells can be suppressed by the short isoform of the long non-coding RNA (lncRNA) nuclear enriched abundant transcript 1 (NEAT1.1). This study investigated whether C/EBPα-p42 or the "mutated" p30 isoforms directly regulate NEAT1.1 or the long isoform NEAT1.2 during differentiation. Material and methods: In 184 Results: NEAT1 shows significantly higher expression in wild-type CEBPA patients than in mutated CEBPA patients. Conclusions: NEAT1.1 is regulated by C/EBPα in AML. Consequently, a mutation in the CEBPA gene not only influences direct targets in gene regulation but also affects targets regulated by NEAT1.1.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.