ArticleLeukemia2015
Detailed analysis of therapy-driven clonal evolution of TP53 mutations in chronic lymphocytic leukemia.
Article in Leukemia, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 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.
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Who cites it
82 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Guideline
- Trial
- Evaluation of 230 patients with relapsed/refractory deletion 17p chronic lymphocytic leukaemia treated with ibrutinib from 3 clinical trials.British journal of haematology · 2018Trial
- Off-trial outcomes of zanubrutinib in Waldenström macroglobulinemia: the prognostic impact of CXCR4 and TP53 alterations.Leukemia · 2026Article
- Prolymphocytic Progression in Chronic Lymphocytic Leukemia Without Richter Transformation: An Eighteen-Year Clinical-Diagnostic Correlation.Case reports in hematology · 2026Article
- PRICKLE3 protects VANGL proteins from CK1-mediated phosphorylation and RNF43-mediated degradation.Communications biology · 2025Article
- Clonal hematopoiesis of indeterminate potential: a multisystem hub bridging hematopoietic dysfunction with non-hematopoietic diseases.Military Medical Research · 2025Review
- Deletion of 17p in cancers: Guilt by (p53) association.Oncogene · 2025Review
- The importance ofMolecular biology research communications · 2025Review
- Recent Advances in the Molecular Biology of Chronic Lymphocytic Leukemia: How to Define Prognosis and Guide Treatment.Cancers · 2024Review
- Unveiling the dynamics and molecular landscape of a rare chronic lymphocytic leukemia subpopulation driving refractoriness: insights from single-cell RNA sequencing.Molecular oncology · 2024Article
- Role of ciliopathy protein TMEM107 in eye development: insights from a mouse model and retinal organoid.Life science alliance · 2023Article
- Unresolved questions in selection of therapies for treatment-naïve chronic lymphocytic leukemia.Journal of hematology & oncology · 2023Review
- Accumulation of STR-Loci Aberrations in Subclones of Jurkat Cell Line as a Model of Tumor Clonal Evolution.Genes · 2023Article
- Distinct p53 phosphorylation patterns in chronic lymphocytic leukemia patients are reflected in the activation of circumjacent pathways upon DNA damage.Molecular oncology · 2023Article
- The Broad Spectrum ofHuman mutation · 2023Article
- Precision diagnostics in chronic lymphocytic leukemia: Past, present and future.Frontiers in oncology · 2023Review
- The spectrum of subclonal TP53 mutations in chronic lymphocytic leukemia: A next generation sequencing retrospective study.Hematological oncology · 2022Article
- Article
- Evolution of TP53 abnormalities during CLL disease course is associated with telomere length changes.BMC cancer · 2022Article
22 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
18 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In chronic lymphocytic leukemia (CLL), the worst prognosis is associated with TP53 defects with the affected patients being potentially directed to alternative treatment. Therapy administration was shown to drive the selection of new TP53 mutations in CLL. Using ultra-deep next-generation sequencing (NGS), we performed a detailed analysis of TP53 mutations' clonal evolution. We retrospectively analyzed samples that were assessed as TP53-wild-type (wt) by FASAY from 20 patients with a new TP53 mutation detected in relapse and 40 patients remaining TP53-wt in relapse. Minor TP53-mutated subclones were disclosed in 18/20 patients experiencing later mutation selection, while only one minor-clone mutation was observed in those patients remaining TP53-wt (n=40). We documented that (i) minor TP53 mutations may be present before therapy and may occur in any relapse; (ii) the majority of TP53-mutated minor clones expand to dominant clone under the selective pressure of chemotherapy, while persistence of minor-clone mutations is rare; (iii) multiple minor-clone TP53 mutations are common and may simultaneously expand. In conclusion, patients with minor-clone TP53 mutations carry a high risk of mutation selection by therapy. Deep sequencing can shift TP53 mutation identification to a period before therapy administration, which might be of particular importance for clinical trials.
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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.