ArticleBlood2017
Inhibition of Pol I transcription treats murine and human AML by targeting the leukemia-initiating cell population.
Article in Blood, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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Who cites it
55 citing papers in PubMed.
- Novel RNA polymerase I and cyclin-dependent kinase combination therapy for the treatment of aggressive acute myeloid leukemia.Leukemia · 2026Article
- The Nucleolus in Human Disease: Ribosome Biogenesis, Nucleolar Surveillance, and Therapeutic Opportunities.Biomolecules · 2026Review
- Toosendanin suppresses acute myeloid leukemia by targeting DDX5/c-Myc axis to inhibit protein synthesis.Journal of translational medicine · 2026Article
- Investigation of the expression and potential mechanistic role of BYSL in acute myeloid leukemia.Clinical and experimental medicine · 2026Article
- AML Disparities Across Racial Ancestry Groups: A Spotlight on the NPM1 Mutations.International journal of molecular sciences · 2026Review
- Targeting RNA polymerase I to boost natural killer cell anticancer activity in multiple myeloma.Cell death & disease · 2025Article
- G-quadruplex stabilization induces DNA breaks in pericentromeric repetitive DNA sequences in B lymphocytes.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Prospective Isolation According to Melanin Pigment Content of Melanoma Cells With Heterogeneous Potentials for Disease Propagation.Pigment cell & melanoma research · 2025Article
- The G-quadruplex ligand CX-5461: an innovative candidate for disease treatment.Journal of translational medicine · 2025Review
- The natural alkaloid nitidine chloride targets RNA polymerase I to inhibit ribosome biogenesis and repress cancer cell growth.Cell death discovery · 2025Article
- Small nucleolar RNAs: the hidden precursors of cancer ribosomes.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2025Review
- Fusion-specific chromatin profiles mediate transcriptional heterogeneity in MLL-rearranged acute lymphoblastic leukemia.Blood advances · 2025Article
- Ribosome biogenesis and ribosomal proteins in cancer stem cells: a new therapeutic prospect.Molecular biology reports · 2024Review
- Article
- Phase separation-competent FBL promotes early pre-rRNA processing and translation in acute myeloid leukaemia.Nature cell biology · 2024Article
- Targeting the ribosome to treat multiple myeloma.Molecular therapy. Oncology · 2024Article
- CX‑5461 potentiates imatinib‑induced apoptosis in K562 cells by stimulatingExperimental and therapeutic medicine · 2024Article
- VAV2 orchestrates the interplay between regenerative proliferation and ribogenesis in both keratinocytes and oral squamous cell carcinoma.Scientific reports · 2024Article
- Low doses of IFN-γ maintain self-renewal of leukemia stem cells in acute myeloid leukemia.Oncogene · 2023Article
- Persistence ofEJHaem · 2023Article
Corrections and comments
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Authors and funding
30 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Despite the development of novel drugs, the prospects for many patients with acute myeloid leukemia (AML) remain dismal. This study reveals that the selective inhibitor of RNA polymerase I (Pol I) transcription, CX-5461, effectively treats aggressive AML, including mixed-lineage leukemia-driven AML, and outperforms standard chemotherapies. In addition to the previously characterized mechanism of action of CX-5461 (ie, the induction of p53-dependent apoptotic cell death), the inhibition of Pol I transcription also demonstrates potent efficacy in p53null AML in vivo. This significant survival advantage in both p53WT and p53null leukemic mice treated with CX-5461 is associated with activation of the checkpoint kinases 1/2, an aberrant G2/M cell-cycle progression and induction of myeloid differentiation of the leukemic blasts. The ability to target the leukemic-initiating cell population is thought to be essential for lasting therapeutic benefit. Most strikingly, the acute inhibition of Pol I transcription reduces both the leukemic granulocyte-macrophage progenitor and leukemia-initiating cell (LIC) populations, and suppresses their clonogenic capacity. This suggests that dysregulated Pol I transcription is essential for the maintenance of their leukemia-initiating potential. Together, these findings demonstrate the therapeutic utility of this new class of inhibitors to treat highly aggressive AML by targeting LICs.
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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.