The evolutionary landscape of chronic lymphocytic leukemia treated with ibrutinib targeted therapy
Open accessAbstract
Treatment of chronic lymphocytic leukemia (CLL) has shifted from chemo-immunotherapy to targeted agents. To define the evolutionary dynamics induced by targeted therapy in CLL, we perform serial exome and transcriptome sequencing for 61 ibrutinib-treated CLLs. Here, we report clonal shifts (change >0.1 in clonal cancer cell fraction, Q < 0.1) in 31% of patients during the first year of therapy, associated with adverse outcome. We also observe transcriptional downregulation of pathways mediating energy metabolism, cell cycle, and B cell receptor signaling. Known and previously undescribed mutations in BTK and PLCG2, or uncommonly, other candidate alterations are present in seventeen subjects at the time of progression. Thus, the frequently observed clonal shifts during the early treatment period and its potential association with adverse outcome may reflect greater evolutionary capacity, heralding the emergence of drug-resistant clones.
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Duration of response with a BTKi is longer in settings where clonal complexity and evolutionary potential are lower, such as in treatment-naïve cases.
“Duration of response with a BTKi is longer in settings where clonal complexity and evolutionary potential are lower, such as in treatment-naïve cases(12, 14, 17).”
From Resistance Mechanisms and Approach to Chronic Lymphocytic Leukemia after BTK Inhibitor Therapy (2025) · cites this paper as [17]
The Results section, “Early clonal shifts associate with adverse clinical outcome,” links clonal shifts to shorter time to progression on ibrutinib. The Discussion says clonal complexity is expected to be lower in treatment-naïve CLL and proposes studying ibrutinib in that setting. It does not establish that treatment-naïve patients have a longer duration of response; that part of the claim turns the paper’s rationale into a demonstrated outcome. (LLM, conf=0.86)
Experimental — accuracy not yet measuredContinuous BTKi therapy exerts a strong selective pressure, with resistant subclones often emerging after years of treatment.
“Likewise, continuous BTKi therapy exerts a strong selective pressure, with resistant subclones often emerging after years of treatment(12, 17, 18).”
From Resistance Mechanisms and Approach to Chronic Lymphocytic Leukemia after BTK Inhibitor Therapy (2025) · cites this paper as [17]
After Ibrutinib treatment, CLL progression favored the selection of rare subclones bearing PLCγ2 mutations.
“However, after Ibrutinib treatment, it was observed that CLL progression favored the selection of rare subclones bearing PLCγ2 mutations (129, 130).”
From The role of PLCγ2 in immunological disorders, cancer, and neurodegeneration (2021) · cites this paper as [129]
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“However, after Ibrutinib treatment, it was observed that CLL progression favored the selection of rare subclones bearing PLCγ2 mutations (129, 130).”
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- Authors
- Landau, D. A., Sun, C., Rosebrock, D., Herman, S. E. M., Fein, J., Sivina, M., Underbayev, C., Liu, D., Hoellenriegel, J., Ravichandran, S., Farooqui, M. Z. H., Zhang, W., Cibulskis, C., Zviran, A., Neuberg, D. S., Livitz, D., Bozic, I., Leshchiner, I., Getz, G., Burger, J. A., Wiestner, A., & Wu, C. J.
- Affiliations
- Broad Institute (US)
- National Institutes of Health (US)
- Tel Aviv University (IL)
- The University of Texas MD Anderson Cancer Center (US)
- Frederick National Laboratory for Cancer Research (US)
- Dana-Farber Cancer Institute (US)
- New York Genome Center (US)
- Corresponding author
- Wiestner, Adrian
- Wu, Catherine J.
- ORCID
- Venue
- Nature Communications
- Published
- 2017-12-19
- Volume
- 8
- Issue
- 1
- Pages
- 2185-2185
- ISSN
- 2041-1723 (ISSN-L)
- PMC
- PMC5736707
- OpenAlex
- W2773946416
- Cited by
- 176
- References
- 53
- Citations by year
- 2026: 3 · 2025: 10 · 2024: 19 · 2023: 19 · 2022: 16 · 2021: 30 · 2020: 28 · 2019: 34 · 2018: 16
- FWCI
- 12.41
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Nature Communications (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Digital Access to Scholarship at Harvard (DASH) (Harvard University) (submittedVersion, cc-by)
- RePEc: Research Papers in Economics (submittedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- American Association for Cancer Research
- Burroughs Wellcome Fund
- Leukemia and Lymphoma Society
- Entertainment Industry Foundation
- Broad Institute (U54HG003067)
- National Institutes of Health
- Stand Up To Cancer
- National Heart, Lung, and Blood Institute (R01HL116452, R01HL131768)
- National Human Genome Research Institute (U54HG003067)
- National Cancer Institute (U10CA180861, R01CA184922, R01CA216273, R01CA182461, P01CA206978)
- National Institute of Environmental Health Sciences (K01ES025431)
- Topics
- Health Sciences › Medicine › Genetics › Chronic Lymphocytic Leukemia Research
- Health Sciences › Medicine › Pathology and Forensic Medicine › Lymphoma Diagnosis and Treatment
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer Genomics and Diagnostics
- Keywords
- chronic lymphocytic leukemia, ibrutinib, clonal evolution, drug resistance, BTK mutations, PLCG2 mutations, B cell receptor signaling, energy metabolism, cell cycle, transcriptome, exome sequencing, treatment outcomes
- MeSH terms
- Rituximab, Exome Sequencing, Agammaglobulinaemia Tyrosine Kinase, Adenine, Adult, Aged, Aged, 80 and over, Antineoplastic Combined Chemotherapy Protocols, Female, Humans, Longitudinal Studies, Male, Middle Aged, Mutation, Piperidines, Prognosis, Protein-Tyrosine Kinases, Pyrazoles, Pyrimidines, Signal Transduction, Leukemia, Lymphocytic, Chronic, B-Cell, Down-Regulation, Gene Expression Regulation, Neoplastic, Treatment Outcome, Disease Progression, Drug Resistance, Neoplasm, Phospholipase C gamma, Molecular Targeted Therapy, Clonal Evolution
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