ArticleCell stem cell2014
Telomerase inhibition effectively targets mouse and human AML stem cells and delays relapse following chemotherapy.
Article in Cell stem cell, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 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
54 citing papers in PubMed, 85 citations in OpenAlex.
- Modulation of the clonal burden in patients with lower-risk myelodysplastic neoplasms treated with imetelstat.Leukemia · 2026Trial
- No Effect of Immunogenicity on Pharmacokinetics, Efficacy, and Safety of the Oligonucleotide Telomerase Inhibitor Imetelstat in Lower-Risk Myelodysplastic Syndromes.Clinical and translational science · 2025Trial
- Low Proarrhythmic Risk of Imetelstat, a Novel Oligonucleotide Telomerase Inhibitor: A Translational Analysis.Clinical and translational science · 2025Trial
- Imetelstat-mediated alterations in fatty acid metabolism to induce ferroptosis as a therapeutic strategy for acute myeloid leukemia.Nature cancer · 2024Trial
- Rapid loss of viability in acute myeloid leukemia cells upon telomerase inactivation.Blood advances · 2026Article
- EomesoderminImmunity · 2025Article
- The interplay of DNA damage, epigenetics and tumour heterogeneity in driving cancer cell fitness.Nature communications · 2025Review
- Population pharmacokinetics of imetelstat, a first-in-class oligonucleotide telomerase inhibitor.CPT: pharmacometrics & systems pharmacology · 2024Article
- Regulation of telomerase towards tumor therapy.Cell & bioscience · 2023Review
- Emerging and Future Targeted Therapies for Pediatric Acute Myeloid Leukemia: Targeting the Leukemia Stem Cells.Biomedicines · 2023Review
- Telomerase RNA component lncRNA as potential diagnostic biomarker promotes CRC cellular migration and apoptosis evasion via modulation of β-catenin protein level.Non-coding RNA research · 2023Article
- The interplay between telomeric complex members and BCR::ABL1 oncogenic tyrosine kinase in the maintenance of telomere length in chronic myeloid leukemia.Journal of cancer research and clinical oncology · 2023Article
- Modelling acute myeloid leukemia (AML): What's new? A transition from the classical to the modern.Drug delivery and translational research · 2023Review
- The telomerase inhibitor imetelstat differentially targets JAK2V617F versus CALR mutant myeloproliferative neoplasm cells and inhibits JAK-STAT signaling.Frontiers in oncology · 2023Article
- A perspective of immunotherapy for acute myeloid leukemia: Current advances and challenges.Frontiers in pharmacology · 2023Review
- In Vitro and In Vivo Modeling of Normal and Leukemic Bone Marrow Niches: Cellular Senescence Contribution to Leukemia Induction and Progression.International journal of molecular sciences · 2022Review
- Imetelstat Induces Leukemia Stem Cell Death in Pediatric Acute Myeloid Leukemia Patient-Derived Xenografts.Journal of clinical medicine · 2022Article
- CircRNF220, not its linear cognate gene RNF220, regulates cell growth and is associated with relapse in pediatric acute myeloid leukemia.Molecular cancer · 2021Article
- Telomerase (Genes · 2021Article
- T-cell-based immunotherapy of acute myeloid leukemia: current concepts and future developments.Leukemia · 2021Review
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Authors and funding
17 authors at 9 institutions in 4 countries.
Funding
Abstract
Acute myeloid leukemia (AML) is an aggressive and lethal blood cancer maintained by rare populations of leukemia stem cells (LSCs). Selective targeting of LSCs is a promising approach for treating AML and preventing relapse following chemotherapy, and developing such therapeutic modalities is a key priority. Here, we show that targeting telomerase activity eradicates AML LSCs. Genetic deletion of the telomerase subunit Terc in a retroviral mouse AML model induces cell-cycle arrest and apoptosis of LSCs, and depletion of telomerase-deficient LSCs is partially rescued by p53 knockdown. Murine Terc(-/-) LSCs express a specific gene expression signature that can be identified in human AML patient cohorts and is positively correlated with patient survival following chemotherapy. In xenografts of primary human AML, genetic or pharmacological inhibition of telomerase targets LSCs, impairs leukemia progression, and delays relapse following chemotherapy. Altogether, these results establish telomerase inhibition as an effective strategy for eliminating AML LSCs.
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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.