ArticleClinical cancer research : an official journal of the American Association for Cancer Research2014
Omacetaxine: a protein translation inhibitor for treatment of chronic myelogenous leukemia.
Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers, 1 of them a synthesis that pooled it.
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Who cites it
74 citing papers in PubMed, 1 synthesis or guideline pooled it, 124 citations in OpenAlex.
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- Homoharringtonine is highly effective against SARS-CoV-2: a potential first-line defense in future coronavirus epidemics.National science review · 2025Article
- Omacetaxine and venetoclax in relapsed/refractory acute myeloid leukemia or myelodysplastic syndrome with mutant RUNX1.Blood neoplasia · 2025Article
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- Homoharringtonine: mechanisms, clinical applications and research progress.Frontiers in oncology · 2025Review
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- Decoding RNA Metabolism by RNA-linked CRISPR Screening in Human Cells.bioRxiv : the preprint server for biology · 2024Article
- MILIP Binding to tRNAs Promotes Protein Synthesis to Drive Triple-Negative Breast Cancer.Cancer research · 2024Article
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- Decoding Ribosome Heterogeneity: A New Horizon in Cancer Therapy.Biomedicines · 2024Review
- Therapeutic options for chronic myeloid leukemia following the failure of second-generation tyrosine kinase inhibitor therapy.Frontiers in oncology · 2024Review
- Targeting Translation and the Cell Cycle Inversely Affects CTC Metabolism but Not Metastasis.Cancers · 2023Article
- A super-enhancer-regulated RNA-binding protein cascade drives pancreatic cancer.Nature communications · 2023Article
14 more citing papers are in PubMed but not listed here.
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Chronic myelogenous leukemia (CML) is driven by the Bcr-Abl fusion protein, which is a result of a (9;22) chromosomal translocation. Imatinib, dasatinib, and nilotinib (tyrosine kinase inhibitors, TKI) have revolutionized how CML is treated. Although the majority of patients respond to these kinase inhibitors, a subset becomes resistant to these therapeutics. Synribo (omacetaxine mepesuccinate) was recently approved by the U.S. Food and Drug Administration for Philadelphia-positive CML either in the chronic or the accelerated phase whose disease failed two prior TKIs. With omacetaxine 1.25 mg/m(2) twice daily for 14 days during induction and for 7 days during maintenance, a major cytogenetic response occurred in 20% of patients in the chronic phase and major hematologic response in 27% of patients in the accelerated phase. Laboratory investigations unraveled the mechanism of action and effectiveness of this agent. Bcr-Abl protein is intrinsically programmed to turn over with a short half-life that makes it susceptible to protein translation inhibitors. Omacetaxine (homoharringtonine) inhibits total protein biosynthesis by binding to A-site cleft of ribosomes. As a corollary to this action, there is a diminution of short-lived proteins, such as Bcr-Abl, followed by cell death. Approval of this first-in-class protein translation inhibitor opens up new avenues for its use in other diseases as well as mechanism-based combinations.
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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.