ArticleNature genetics2026
CDK4/6 inhibition mitigates chemotherapy-induced expansion of TP53-mutant clonal hematopoiesis.
Article in Nature genetics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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
11 citing papers in PubMed.
- Finding clonal hematopoiesis before sequencing.Blood advances · 2026Article
- Clinical management of clonal hematopoiesis.Cancer · 2026Review
- Article
- Programmed Clonal Expansion Associated with V(D)J Recombination Drives an ATM-Dependent Vulnerability Underlying Preferential Lymphocyte Depletion and Myeloid Bias Following DNA Damage.bioRxiv : the preprint server for biology · 2026Article
- DNMT3A variants are associated with the development of nodal TFH cell lymphoma, angioimmunoblastic-type after solid tumour occurrence.British journal of haematology · 2026Article
- Evolution of clonal hematopoiesis during cancer treatment and its impact on outcomes.The Journal of clinical investigation · 2026Article
- CDK4/6 Inhibitor-Induced Senescence in Cancer: Mechanisms and Therapeutic Implications.Cancers · 2026Review
- Clonal hematopoiesis in patients with cancer and cancer survivors: From clonal burden to cardiovascular diseases.Cancer · 2026Review
- Clonal hematopoiesis and its progression to myeloid neoplasms: insights into risk, biology, and therapeutic strategies.Haematologica · 2026Review
- CDK4/6 inhibition mitigates chemotherapy-induced expansion of TP53-mutant clonal hematopoiesis.Nature genetics · 2026Article
- The therapy-conditioned host: a state-transition framework for second primary cancer evolution.Frontiers in oncology · 2026Article
Corrections and comments
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Authors and funding
18 authors.
Funding
Abstract
Therapy-related myeloid neoplasm (tMN) is a fatal consequence of exposure to cytotoxic therapy administered in the treatment of cancer. Individuals with pre-existing TP53 clonal hematopoiesis (CH) are at high risk of tMN, with avoidance of therapy being the only strategy to reduce tMN risk. Here, in four randomized clinical trials, we show that the CDK4/6 inhibitor trilaciclib, given in conjunction with a variety of chemotherapeutic regimens and across diverse populations of patients with cancer, mitigates chemotherapy-related expansion of CH clones with mutations in DNA damage response genes, including TP53. This finding was also observed in a syngeneic mouse model of TP53-mutant CH, demonstrating that CDK4/6 inhibition blocks platinum-induced TP53 competitive repopulation through promoting hematopoietic stem and progenitor quiescence and decreasing the stemness advantage of TP53-mutant clones. This represents a proof of concept for a potential pharmacologic strategy to block chemotherapy-induced expansion of preleukemic TP53-mutant clones.
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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.