ReviewInternational journal of molecular sciences2025
Chronic Myeloid Leukemia and the T315I
Review in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
6 citing papers in PubMed.
- Targeting ABL Tyrosine Kinase in Chronic Myeloid Leukemia: Design, Synthesis, Biological Evaluation, and Computational Studies of Novel Thiazolone Derivatives.Pharmaceutics · 2026Article
- Design, Synthesis, and Biological Evaluation ofPharmaceuticals (Basel, Switzerland) · 2026Article
- Evolving Therapeutic Algorithms in Chronic Myeloid Leukemia: Integrating Efficacy, Safety, and Survivorship.Biomedicines · 2026Review
- Advances in Targeting BCR-ABLMolecules (Basel, Switzerland) · 2026Review
- Targeting leukemic stem and progenitor cells expressing different BCR::ABL1 levels: antileukemic activity of asciminib with or without TKIs.Frontiers in pharmacology · 2026Article
- Bone Marrow Edema and Tyrosine Kinase Inhibitors Treatment in Chronic Myeloid Leukemia.Diagnostics (Basel, Switzerland) · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic myeloid leukemia (CML) is a myeloproliferative neoplasm characterized by both an abnormal expansion of the granuloblastic clone and the pathognomonic presence of the Philadelphia (Ph) chromosome that generates the BCR::ABL1 oncoprotein. Despite the surfacing of tyrosine kinase Inhibitors (TKIs) in 2001, which changed the evolution of the disease, resistance due to point mutation or compound alteration during treatment with target therapy may occur. One of the mutations that is still an on-going challenge in clinical and scientific field is the T315I mutation, since it gives patients a poor prognosis attributable to acquired resistance to therapy. In the following narrative review, we will discuss the current knowledge on the T315I mutation, explore the most suitable treatment options, examine the role of third-generation tyrosine kinase inhibitors, and outline potential future therapeutic strategies.
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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.