ArticleLeukemia2025
YTHDC1 is a therapeutic target for B-cell acute lymphoblastic leukemia by attenuating DNA damage response through the KMT2C-H3K4me1/me3 epigenetic axis.
Article in Leukemia, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
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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
14 citing papers in PubMed.
- A positive feedback loop between YTHDC1 and EP300 drives multiple myeloma tumorigenesis.Oncogene · 2026Article
- Natural Plant Bioactives as Regulators of Histone Modifications: Bridging Epigenetics and Anticancer Therapy.Phytotherapy research : PTR · 2026Review
- Article
- mPharmaceuticals (Basel, Switzerland) · 2026Review
- Low YTHDC1 Expression Upregulates FSCN1 to Promote Nuclear F-Actin Formation and Facilitate Double-strand DNA Breaks Repair in TMZ-Resistant Glioblastoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Emerging role of RNA modification reader YTHDF2 in hematopoiesis, immunity, and cancer.MedScience · 2026Review
- Diverse roles of YTHDC1 in chromatin and blood cancers.Frontiers in genetics · 2026Review
- mActa pharmaceutica Sinica. B · 2025Review
- Age-Driven Genetic and Epigenetic Heterogeneity in B-ALL.International journal of molecular sciences · 2025Review
- The Dynamic Interactions of m6A Modification and R-Loops: Implications for Genome Stability.Epigenomes · 2025Review
- Development of a cuproptosis-related prognostic signature to reveal heterogeneity of the immune microenvironment and drug sensitivity in acute lymphoblastic leukemia.European journal of medical research · 2025Article
- The m6A revolution: transforming tumor immunity and enhancing immunotherapy outcomes.Cell & bioscience · 2025Review
- Ribosomal protein L9 is a potential therapeutic target for B-ALL through the activation of the p53 signaling pathway.Frontiers in immunology · 2025Article
- Advances in the application of patient-derived xenograft models in acute leukemia resistance.Cancer drug resistance (Alhambra, Calif.) · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors.
Funding
Abstract
B-cell acute lymphoblastic leukemia (B-ALL) is an aggressive malignancy characterized by the aberrant accumulation of immature and dysfunctional B cells in bone marrow (BM). Although chemotherapy and other therapies have been widely applied, some patients such as relapsed or drug-refractory (R/R) B-ALL patients exhibit limited response. YT521-B homologous domain-containing protein 1 (YTHDC1) is a nuclear reader of N
Indexed as
Identifiers
39501105What 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.