ArticleLeukemia2014
Expression of nucleoside-metabolizing enzymes in myelodysplastic syndromes and modulation of response to azacitidine.
Article in Leukemia, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 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.
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Who cites it
49 citing papers in PubMed, 91 citations in OpenAlex.
- Specific molecular signatures predict decitabine response in chronic myelomonocytic leukemia.The Journal of clinical investigation · 2015Trial
- Uridine cytidine kinases govern molnupiravir bioactivation and anti-SARS-CoV-2 activity.PLoS pathogens · 2026Article
- Uridine-Cytidine Kinase 2 (UCK2)/Uridine-Cytidine Kinase Like 1 (UCKL1) complex exacerbates the differentiation of myocardial fibroblasts via TRIM21/Smurf2/Smad3 pathway after myocardial infarction.Molecular biomedicine · 2025Article
- From Chemotherapy to Targeted Therapy: Unraveling Resistance in Acute Myeloid Leukemia Through Genetic and Non-Genetic Insights.International journal of molecular sciences · 2025Review
- Metabolic dysregulation in myelodysplastic neoplasm: impact on pathogenesis and potential therapeutic targets.Medical oncology (Northwood, London, England) · 2024Review
- Venetoclax and Hypomethylating Agent Combination in Myeloid Malignancies: Mechanisms of Synergy and Challenges of Resistance.International journal of molecular sciences · 2023Review
- Review
- DNA methyltransferase inhibitor exposure-response: Challenges and opportunities.Clinical and translational science · 2023Review
- CCRL2 affects the sensitivity of myelodysplastic syndrome and secondary acute myeloid leukemia cells to azacitidine.Haematologica · 2023Article
- Resistance of Leukemia Cells to 5-Azacytidine: Different Responses to the Same Induction Protocol.Cancers · 2023Article
- Therapeutic Targets in Myelodysplastic Neoplasms: Beyond Hypomethylating Agents.Current hematologic malignancy reports · 2023Review
- What's Next after Hypomethylating Agents Failure in Myeloid Neoplasms? A Rational Approach.Cancers · 2023Review
- Understanding the Continuum between High-Risk Myelodysplastic Syndrome and Acute Myeloid Leukemia.International journal of molecular sciences · 2023Review
- Ubiquitin-specific protease 28: the decipherment of its dual roles in cancer development.Experimental hematology & oncology · 2023Review
- Solute Carrier Family 29A1 Mediates In Vitro Resistance to Azacitidine in Acute Myeloid Leukemia Cell Lines.International journal of molecular sciences · 2023Article
- Combination of Tissue Microarray Profiling and Multiplexed IHC Approaches to Investigate Transport Mechanism of Nucleoside Analog Drug Resistance.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Different Gene Sets Are Associated With Azacitidine Response In Vitro Versus in Myelodysplastic Syndrome Patients.HemaSphere · 2022Article
- Epigenetic Silencing ofInternational journal of molecular sciences · 2022Article
- Adult T-cell leukemia-lymphoma acquires resistance to DNA demethylating agents through dysregulation of enzymes involved in pyrimidine metabolism.International journal of cancer · 2022Article
- The roles of KLHL family members in human cancers.American journal of cancer research · 2022Review
Corrections and comments
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Authors and funding
15 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The nucleoside analog azacitidine (AZA) is used in the treatment of myelodysplastic syndromes (MDS), but 30-40% of patients fail to respond or relapse after treatment. Hence, to identify new molecular alterations that allow for identification of patients unlikely to respond to AZA could impact the utility of this therapy. We determined the expression levels of genes involved in AZA metabolism: UCK1, UCK2, DCK, hENT1, RRM1 and RRM2 using quantitative PCR in samples from 57 patients with MDS who received AZA. Lower expression of UCK1 was seen in patients without a response to AZA (median 0.2 vs 0.49 for patients with response to AZA, P=0.07). This difference in UCK1 expression was not influenced by aberrant methylation of the UCK1 promoter. In addition, the seven polymorphic loci found in the coding sequence were not associated with UCK1 gene expression nor AZA response. Silencing of UCK1 by siRNA leads to blunted response to AZA in vitro. The univariate analysis revealed that patients expressing lower than median levels of UCK1 had a shorter overall survival (P=0.049). Our results suggest that expression level of UCK1 is correlated with clinical outcome and may influence the clinical response to AZA treatment in patients with MDS.
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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 OpenQuestion graph.