ReviewJournal of hematology & oncology2021
Third-line therapy for chronic myeloid leukemia: current status and future directions.
Review in Journal of hematology & oncology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers, 3 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
65 citing papers in PubMed, 3 syntheses or guidelines pooled it, 113 citations in OpenAlex.
- Exploring the mechanisms and therapeutic role of γ-oryzanol in neuropathic pain: a systematic review.Inflammopharmacology · 2026Pooled it
- Tyrosine kinase inhibitors for chronic myeloid leukemia: a landscape analysis of global clinical trials based on public registries.Frontiers in pharmacology · 2026Pooled it
- A Systematic Literature Review of the Economic Evaluations of Treatments for Patients with Chronic Myeloid Leukemia.PharmacoEconomics · 2022Pooled it
- Trial
- Asciminib in patients with newly diagnosed chronic myeloid leukemia: results from the Japanese subgroup of ASC4FIRST.International journal of hematology · 2025Trial
- Asciminib remained superior vs bosutinib in late-line CML-CP after nearly 4 years of follow-up in ASCEMBL.Blood advances · 2025Trial
- Exposure-response analysis of asciminib efficacy and safety in patients with chronic myelogenous leukemia in chronic phase.Cancer chemotherapy and pharmacology · 2025Trial
- Trial
- Trial
- Population Pharmacokinetics of Asciminib in Tyrosine Kinase Inhibitor-Treated Patients with Philadelphia Chromosome-Positive Chronic Myeloid Leukemia in Chronic and Acute Phases.Clinical pharmacokinetics · 2022Trial
- Asciminib monotherapy in patients with BCR::ABL1 T315I-mutated chronic-phase chronic myeloid leukemia: phase 1 trial final results.Leukemia · 2026Article
- Postmarketing surveillance study of asciminib in patients with resistant/intolerant chronic myeloid leukemia in Japan.International journal of hematology · 2026Article
- Review
- Inhibition of Pellino-1 reverts the progression and tyrosine kinase inhibitor resistance in chronic myeloid leukemia.Cell death & disease · 2026Article
- Article
- Article
- Potential utility of PPARγ agonists in targeting chronic myeloid leukemia stem cells.Annals of hematology · 2026Article
- Dual Proteasome and Histone Deacetylase Inhibition Overcomes Tyrosine Kinase Inhibitor Resistance in Breakpoint Cluster Region: Abelson 1-Driven Leukaemia Cell Lines.Journal of cellular and molecular medicine · 2026Article
- Fusion oncoproteins orchestrate tumorigenesis and sustain malignant progression via a positive feedback mechanism.Cell & bioscience · 2026Review
- Case Report: Pediatric Philadelphia chromosome-positive T-lymphoblastic leukemia relapsing as chronic-phase CML after treatment discontinuation.Frontiers in oncology · 2026Article
5 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic myeloid leukemia (CML) is driven by the BCR-ABL1 fusion protein, formed by a translocation between chromosomes 9 and 22 that creates the Philadelphia chromosome. The BCR-ABL1 fusion protein is an optimal target for tyrosine kinase inhibitors (TKIs) that aim for the adenosine triphosphate (ATP) binding site of ABL1. While these drugs have greatly improved the prognosis for CML, many patients ultimately fail treatment, some requiring multiple lines of TKI therapy. Mutations can occur in the ATP binding site of ABL1, causing resistance by preventing the binding of many of these drugs and leaving patients with limited treatment options. The approved TKIs are also associated with adverse effects that may lead to treatment discontinuation in some patients. Efficacy decreases with each progressive line of therapy; data suggest little clinical benefit of treatment with a third-line (3L), second-generation tyrosine kinase inhibitor (2GTKI) after failure of a first-generation TKI and a 2GTKI. Novel treatment options are needed for the patient population that requires treatment in the 3L setting and beyond. This review highlights the need for clear guidelines and new therapies for patients requiring 3L treatment and beyond.
Indexed as
Identifiers
What OpenQuestion holds
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.