ArticleHaematologica2022
Clonal evolution in chronic lymphocytic leukemia is scant in relapsed but accelerated in refractory cases after chemo(immune) therapy.
Article in Haematologica, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- Mutational and copy number analysis at diagnosis and relapse of mantle cell lymphoma.Haematologica · 2026Article
- DNA methylation-based classification of hematolymphoid neoplasms.Blood advances · 2026Article
- The molecular map of CLL and Richter's syndrome.Seminars in hematology · 2024Review
- Targeting the NTSR2/TrkB oncogenic pathway in chronic lymphocytic leukemia.Scientific reports · 2024Article
- Genetic Lesions in Russian CLL Patients with the Most Common Stereotyped Antigen Receptors.Genes · 2023Article
- Integrative Approaches of DNA Methylation Patterns According to Age, Sex and Longitudinal Changes.Current genomics · 2023Article
- Article
- The EHA Research Roadmap: Malignant Lymphoid Diseases.HemaSphere · 2022Article
- The Determinants of B Cell Receptor Signaling as Prototype Molecular Biomarkers of Leukemia.Frontiers in oncology · 2021Article
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Clonal evolution is involved in the progression of chronic lymphocytic leukemia (CLL). In order to link evolutionary patterns to different disease courses, we performed a long-term longitudinal mutation profiling study of CLL patients. Tracking somatic mutations and their changes in allele frequency over time and assessing the underlying cancer cell fraction revealed highly distinct evolutionary patterns. Surprisingly, in long-term stable disease and in relapse after long-lasting clinical response to treatment, clonal shifts are minor. In contrast, in refractory disease major clonal shifts occur although there is little impact on leukemia cell counts. As this striking pattern in refractory cases is not linked to a strong contribution of known CLL driver genes, the evolution is mostly driven by treatment-induced selection of sub-clones, underlining the need for novel, non-genotoxic treatment regimens.
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