ArticleFrontiers in oncology2023
Clonal evolution in tyrosine kinase inhibitor-resistance: lessons from
Article in Frontiers in oncology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- Article
- Advancing chronic myeloid leukemia research with next-generation sequencing: potential benefits, limitations, and future clinical integration.Human genetics · 2025Review
- Association of fibronectin 1 deregulation with tyrosine kinase inhibitor resistance in chronic myeloid leukemia.Frontiers in cell and developmental biology · 2025Article
- The role of the lysine histone methylase KMT2D in chronic myeloid leukemia.Frontiers in pharmacology · 2025Article
- BTK acts as a modulator of the response to imatinib in chronic myeloid leukemia.Oncology letters · 2024Article
- Synthesis of Novel Nilotinib Analogues and Biological Evaluation of Their Antiplatelet Activity and Functionality towards Cancer Cell Proliferation In Vitro.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Molecular biomarkers of leukemia: convergence-based drug resistance mechanisms in chronic myeloid leukemia and myeloproliferative neoplasms.Frontiers in pharmacology · 2024Review
- Chromosomal Copy Number Variation Predicts EGFR-TKI Response and Prognosis for Patients with Non-Small Cell Lung Cancer.Pharmacogenomics and personalized medicine · 2023Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Resistance in anti-cancer treatment is a result of clonal evolution and clonal selection. In chronic myeloid leukemia (CML), the hematopoietic neoplasm is predominantly caused by the formation of the BCR::ABL1 kinase. Evidently, treatment with tyrosine kinase inhibitors (TKIs) is tremendously successful. It has become the role model of targeted therapy. However, therapy resistance to TKIs leads to loss of molecular remission in about 25% of CML patients being partially due to BCR::ABL1 kinase mutations, while for the remaining cases, various other mechanisms are discussed. Methods: Here, we established an Results: In this model, acquired sequence variants in Discussion: Our data demonstrate that our
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Registered trials
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