ArticleLeukemia2017
Cytogenetic landscape and impact in blast phase of chronic myeloid leukemia in the era of tyrosine kinase inhibitor therapy.
Article in Leukemia, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 48 citations in OpenAlex.
- Evolving Therapeutic Algorithms in Chronic Myeloid Leukemia: Integrating Efficacy, Safety, and Survivorship.Biomedicines · 2026Review
- A case report of BCR-ABL(+) acute myeloid leukemia and literature review.Frontiers in oncology · 2026Article
- A nomogram for predicting T315I-free survival in chronic phase chronic myeloid leukemia patients: a multicenter retrospective study.Scientific reports · 2025Article
- Impact of additional cytogenetic aberrations at diagnosis of chronic phase chronic myeloid leukemia.Therapeutic advances in medical oncology · 2025Article
- Review
- Erythroid variant evolving from chronic myeloid leukemia resistant to multiple tyrosine kinase inhibitors: a rare case report.Diagnostic pathology · 2024Article
- Prognosis in Chronic Myeloid Leukemia: Baseline Factors, Dynamic Risk Assessment and Novel Insights.Cells · 2023Review
- Chronic Myeloid Leukemia, from Pathophysiology to Treatment-Free Remission: A Narrative Literature Review.Journal of blood medicine · 2023Review
- Treatment of blast phase chronic myeloid leukaemia: A rare and challenging entity.British journal of haematology · 2022Review
- [Analysis of clinical features and prognosis of patients with chronic myelogenous leukemia harboring additional chromosomal abnormalities in Ph-positive cells].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2021Article
- Clonal evolution and clinical implications of genetic abnormalities in blastic transformation of chronic myeloid leukaemia.Nature communications · 2021Article
- Understanding and Monitoring Chronic Myeloid Leukemia Blast Crisis: How to Better Manage Patients.Cancer management and research · 2021Review
- Article
- [The significance of non-Ph chromosome in chronic myelogenous leukemia].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2020Article
- Clonal evolution of AML1-ETO coexisting with BCR-ABL and additional chromosome abnormalities in a blastic transformation of chronic myeloid leukemia.The Journal of international medical research · 2020Article
- Next-generation sequencing for BCR-ABL1 kinase domain mutation testing in patients with chronic myeloid leukemia: a position paper.Journal of hematology & oncology · 2019Review
- Management of Chronic Myeloid Leukemia in Advanced Phase.Frontiers in oncology · 2019Review
- Assessing Measurable Residual Disease in Chronic Myeloid Leukemia. BCR-ABL1 IS in theFrontiers in oncology · 2019Article
- Chronic Myeloid Leukemia: Beyond BCR-ABL1.Current hematologic malignancy reports · 2018Review
- Targeting PFKFB3 sensitizes chronic myelogenous leukemia cells to tyrosine kinase inhibitor.Oncogene · 2018Article
Corrections and comments
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Authors and funding
10 authors at 6 institutions in 2 countries.
Funding
Abstract
The landscape of additional chromosomal alterations (ACAs) and their impact in chronic myeloid leukemia, blast phase (CML-BP) treated with tyrosine kinase inhibitors (TKIs) have not been well studied. Here, we investigated a cohort of 354 CML-BP patients treated with TKIs. We identified +8, an extra Philadelphia chromosome (Ph), 3q26.2 rearrangement, -7 and isochromosome 17q (i(17q)) as the major-route changes with a frequency of over 10%. In addition, +21 and +19 had a frequency of over 5%. These ACAs demonstrated lineage specificity: +8, 3q26.2 rearrangement, i(17q) and +19 were significantly more common in myeloid BP, and -7 more common in lymphoid BP; +Ph and +21 were equally distributed between two groups. Pearson correlation analysis revealed clustering of common ACAs into two groups: 3q26.2 rearrangement, -7 and i(17q) formed one group, and other ACAs formed another group. The grouping correlated with risk stratification of ACAs in CML, chronic phase. Despite the overall negative prognostic impact of ACAs, stratification of ACAs into major vs minor-route changes provided no prognostic relevance in CML-BP. The emergence of 3q26.2 rearrangement as a major-route change in the TKI era correlated with a high frequency of ABL1 mutations, supporting a role for TKI resistance in the changing cytogenetic landscape in CML-BP.
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Registered trials
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