ArticleLeukemia2015
The impact of SF3B1 mutations in CLL on the DNA-damage response.
Article in Leukemia, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 1 of them a synthesis that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
52 citing papers in PubMed, 1 synthesis or guideline pooled it, 89 citations in OpenAlex.
- Prognostic significance of in patients with chronic lymphocytic leukemia: A meta-analysis.Annals of hematology · 2025Pooled it
- Trial
- Cancer-associated SF3B1 mutation suppresses DNA repair by disrupting the organization of nuclear actin network.Cell death & disease · 2026Article
- Distinct and convergent effects ofProceedings of the National Academy of Sciences of the United States of America · 2025Article
- Insights into genetic aberrations and signalling pathway interactions in chronic lymphocytic leukemia: from pathogenesis to treatment strategies.Biomarker research · 2024Review
- Aberrant spliceosome activity via elevated intron retention and upregulation and phosphorylation of SF3B1 in chronic lymphocytic leukemia.Molecular therapy. Nucleic acids · 2024Article
- The molecular map of CLL and Richter's syndrome.Seminars in hematology · 2024Review
- Pan-Cancer Analysis of ART1 and its Potential Value in Gastric Cancer.Journal of Cancer · 2024Article
- Ancistrocladinium A Induces Apoptosis in Proteasome Inhibitor-Resistant Multiple Myeloma Cells: A Promising Therapeutic Agent Candidate.Pharmaceuticals (Basel, Switzerland) · 2023Article
- Article
- Precision diagnostics in chronic lymphocytic leukemia: Past, present and future.Frontiers in oncology · 2023Review
- Proteomic analysis defines the interactome of telomerase in the protozoan parasite,Frontiers in cell and developmental biology · 2023Article
- Multiple Mechanisms of NOTCH1 Activation in Chronic Lymphocytic Leukemia: NOTCH1 Mutations and Beyond.Cancers · 2022Review
- Subclonal heterogeneity sheds light on the transformation trajectory in IGLV3-21Blood cancer journal · 2022Article
- Co-occurrence of BAP1 and SF3B1 mutations in uveal melanoma induces cellular senescence.Molecular oncology · 2022Article
- SF3B1 homeostasis is critical for survival and therapeutic response in T cell leukemia.Science advances · 2022Article
- Recurrent Spliceosome Mutations in Cancer: Mechanisms and Consequences of Aberrant Splice Site Selection.Cancers · 2022Review
- Review
- Article
- Deciphering the nonsense-mediated mRNA decay pathway to identify cancer cell vulnerabilities for effective cancer therapy.Journal of experimental & clinical cancer research : CR · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
20 authors at 7 institutions in 5 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutations or deletions in TP53 or ATM are well-known determinants of poor prognosis in chronic lymphocytic leukemia (CLL), but only account for approximately 40% of chemo-resistant patients. Genome-wide sequencing has uncovered novel mutations in the splicing factor sf3b1, that were in part associated with ATM aberrations, suggesting functional synergy. We first performed detailed genetic analyses in a CLL cohort (n=110) containing ATM, SF3B1 and TP53 gene defects. Next, we applied a newly developed multiplex assay for p53/ATM target gene induction and measured apoptotic responses to DNA damage. Interestingly, SF3B1 mutated samples without concurrent ATM and TP53 aberrations (sole SF3B1) displayed partially defective ATM/p53 transcriptional and apoptotic responses to various DNA-damaging regimens. In contrast, NOTCH1 or K/N-RAS mutated CLL displayed normal responses in p53/ATM target gene induction and apoptosis. In sole SF3B1 mutated cases, ATM kinase function remained intact, and γH2AX formation, a marker for DNA damage, was increased at baseline and upon irradiation. Our data demonstrate that single mutations in sf3b1 are associated with increased DNA damage and/or an aberrant response to DNA damage. Together, our observations may offer an explanation for the poor prognosis associated with SF3B1 mutations.
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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.