ArticleBMC cancer2025
DHX9 as a prognostic biomarker and its biological roles in acute myeloid leukemia.
Article in BMC cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- DHX9 sustains hematopoietic stem cell function in cooperation with H3 acetylation.Stem cell reports · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
backgroundAcute myeloid leukemia (AML) is a highly malignant hematopoietic disease, with low remission and high relapse rates, and there is currently no effective treatment except for acute promyelocytic leukemia. DExH-Box Helicase 9, a member of the DExD/H-box family of helicases, is highly expressed in some solid tumors and associated with poor prognosis. However, its role in AML has not been reported. This study aimed to investigate the clinical significance and biological roles of DHX9 in AML.
methodsSpecific gene primers and TaqMan probes were prepared to construct absolute quantitative methods for DHX9. Receiver operating characteristic curves were constructed to evaluate the diagnostic and prognostic value of DHX9. Series of shRNA-mediated DHX9 knockdown experiments to assess the functional roles of DHX9 such as proliferation, cell cycle, apoptosis and differentiation ability. In addition, bioinformatic analysis was used to find out which potential pathways DHX9 participated in.
resultsA detection method for DHX9 was successfully established. DHX9 was highly expressed in the AML patients with aberrant myeloid blasts. Significant differences were found among patients with different risk levels, with high levels of DHX9 related to a poor prognosis. shRNA-mediated DHX9 knockdown significantly inhibited the proliferation and cell cycle, and induced apoptosis and differentiation in THP-1 and MOLM-13 cells. Further bioinformatic analysis showed that DHX9 expression was significantly associated with metabolism pathways, suggesting that DHX9 may be involved in the metabolic reprogramming of AML blasts.
conclusionsOur study discovers that DHX9 promotes AML development and may serve as a biomarker for AML, holding a better prospect for clinical application.
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.