ReviewHematology/oncology clinics of North America2020
Targeting Aberrant Splicing in Myelodysplastic Syndromes: Biologic Rationale and Clinical Opportunity.
Review in Hematology/oncology clinics of North America, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
5 citing papers in PubMed, 13 citations in OpenAlex.
- U2AF1 in various neoplastic diseases and relevant targeted therapies for malignant cancers with complex mutations (Review).Oncology reports · 2024Review
- Proteomic discovery of chemical probes that perturb protein complexes in human cells.Molecular cell · 2023Article
- Article
- Molecular Threat of Splicing Factor Mutations to Myeloid Malignancies and Potential Therapeutic Modulations.Biomedicines · 2022Review
- New Approaches to Myelodysplastic Syndrome Treatment.Current treatment options in oncology · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Myelodysplastic syndromes are enriched for somatic mutations in the pre-mRNA splicing apparatus, with recurrent acquired mutations most commonly occurring in SF3B1, SRSF2, U2AF1, and ZRSR2. These mutations appear to be early events in the pathogenesis of disease, and, given their frequency and central role in leukemogenesis, are of interest as potential therapeutic targets. Clinical trials are exploring targets that directly affect the spliceosome (splicing modulators or protein arginine methyltransferase 5 inhibitors) or that exploit possible vulnerabilities created by alternative splicing (inhibiting ATR). Future research is needed to explore novel targets and therapeutic combinations and understand how these mutations lead to clonal dominance.
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What 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.