ArticleBlood2022
Lenalidomide promotes the development of TP53-mutated therapy-related myeloid neoplasms.
Article in Blood, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 papers, 3 of them syntheses that pooled it.
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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.
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Who cites it
99 citing papers in PubMed, 3 syntheses or guidelines pooled it, 131 citations in OpenAlex.
- Risk for second primary malignancies in patients with multiple myeloma: a systematic review and meta-analysis.Frontiers in oncology · 2026Pooled it
- Acute lymphoblastic leukemia in patients treated with lenalidomide for multiple myeloma: a safety meta-analysis of randomized controlled trials combined with a retrospective study of the WHO's pharmacovigilance database.Blood cancer journal · 2024Pooled it
- The role of clonal progression leading to the development of therapy-related myeloid neoplasms.Annals of hematology · 2024Pooled it
- A multicenter phase 1/2 trial of lenalidomide and dose-adjusted EPOCH-R in MYC-associated DLBCL.Blood advances · 2025Trial
- Large clones of clonal hematopoiesis affect outcome in mantle cell lymphoma: results from the FIL MCL0208 clinical trial.Blood advances · 2025Trial
- Germ line landscape stratification defines distinct molecular and prognostic groups in therapy-related myeloid neoplasms.Blood advances · 2026Article
- When MRD Is Not MRD: A Context-Dependent Interpretation in Clinical Decision-Making.European journal of haematology · 2026Article
- Clinical management of clonal hematopoiesis.Cancer · 2026Review
- Lenalidomide Exposure andCurrent oncology (Toronto, Ont.) · 2026Review
- Myelodysplastic syndrome with cryptic 5q deletions in young male patients showing sustained response to lenalidomide.Haematologica · 2026Article
- Characteristics and outcomes of secondary hematological malignancies following autologous stem cell transplantation for multiple myeloma.Blood cancer journal · 2026Article
- Identification of two novel TP53 mutations in secondary acute myeloid leukemia following multiple myeloma: a case report.Blood science (Baltimore, Md.) · 2026Article
- Clonal hematopoiesis in patients with cancer and cancer survivors: From clonal burden to cardiovascular diseases.Cancer · 2026Review
- Flare of clonal hematopoiesis, TP53 expansion and prior melphalan drive post-CAR-T myeloid disorders in multiple myeloma.Leukemia · 2026Article
- Clonal hematopoiesis and its progression to myeloid neoplasms: insights into risk, biology, and therapeutic strategies.Haematologica · 2026Review
- Counting the CHIPs: The High-Stakes Role of Clonal Hematopoiesis in Multiple Myeloma.Biomedicines · 2026Review
- Article
- Lenalidomide-associated reversible TP53-mutated clonal hematopoiesis in plasma cell neoplasms.Haematologica · 2026Article
- [Chinese expert consensus on the clinical application of next-generation sequencing technology in myelodysplastic neoplasms (2026)].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2026Article
- The Immunological Consequences of Clonal Hematopoiesis in Heart Failure.Immunological reviews · 2026Review
39 more citing papers are in PubMed but not listed here.
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Authors and funding
25 authors at 7 institutions in 3 countries.
Funding
Abstract
There is a growing body of evidence that therapy-related myeloid neoplasms (t-MNs) with driver gene mutations arise in the background of clonal hematopoiesis (CH) under the positive selective pressure of chemo- and radiation therapies. Uncovering the exposure relationships that provide selective advantage to specific CH mutations is critical to understanding the pathogenesis and etiology of t-MNs. In a systematic analysis of 416 patients with t-MN and detailed prior exposure history, we found that TP53 mutations were significantly associated with prior treatment with thalidomide analogs, specifically lenalidomide. We demonstrated experimentally that lenalidomide treatment provides a selective advantage to Trp53-mutant hematopoietic stem and progenitor cells (HSPCs) in vitro and in vivo, the effect of which was specific to Trp53-mutant HSPCs and was not observed in HSPCs with other CH mutations. Because of the differences in CK1α degradation, pomalidomide treatment did not provide an equivalent level of selective advantage to Trp53-mutant HSPCs, providing a biological rationale for its use in patients at high risk for t-MN. These findings highlight the role of lenalidomide treatment in promoting TP53-mutated t-MNs and offer a potential alternative strategy to mitigate the risk of t-MN development.
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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.