ReviewCurrent hematologic malignancy reports2012
Genetic mechanisms of chronic myeloid leukemia blastic transformation.
Review in Current hematologic malignancy reports, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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
23 citing papers in PubMed, 49 citations in OpenAlex.
- Targeting Musashi-2 to counteract senescence and resistance in chronic myeloid leukemia: enhancing the efficacy of imatinib therapy.BMC cancer · 2025Article
- Utilization of Machine Learning in the Prediction, Diagnosis, Prognosis, and Management of Chronic Myeloid Leukemia.International journal of molecular sciences · 2025Review
- From regulation to deregulation of p53 in hematologic malignancies: implications for diagnosis, prognosis and therapy.Biomarker research · 2024Review
- Review
- Tyrosine Kinase Inhibitor Discontinuation in Chronic Myeloid Leukemia: Strategies to Optimize Success and New Directions.Current hematologic malignancy reports · 2024Review
- Artificial Intelligence-Based Management of Adult Chronic Myeloid Leukemia: Where Are We and Where Are We Going?Cancers · 2024Review
- Enabling biomedical technologies for chronic myelogenous leukemia (CML) biomarkers detection.Biomicrofluidics · 2024Review
- The interplay between telomeric complex members and BCR::ABL1 oncogenic tyrosine kinase in the maintenance of telomere length in chronic myeloid leukemia.Journal of cancer research and clinical oncology · 2023Article
- Resistance to Tyrosine Kinase Inhibitors in Chronic Myeloid Leukemia-From Molecular Mechanisms to Clinical Relevance.Cancers · 2021Review
- BCR/ABL1 fluorescenceHematology reports · 2021Article
- Article
- Understanding and Monitoring Chronic Myeloid Leukemia Blast Crisis: How to Better Manage Patients.Cancer management and research · 2021Review
- Cytogenetic landscape and impact in blast phase of chronic myeloid leukemia in the era of tyrosine kinase inhibitor therapy.Leukemia · 2017Article
- Cellular and Molecular Networks in Chronic Myeloid Leukemia: The Leukemic Stem, Progenitor and Stromal Cell Interplay.Current drug targets · 2017Review
- Illegitimate RAG-mediated recombination events are involved in IKZF1 Δ3-6 deletion in BCR-ABL1 lymphoblastic leukaemia.Clinical and experimental immunology · 2016Article
- Article
- The Philadelphia chromosome in leukemogenesis.Chinese journal of cancer · 2016Review
- Best Practices in Chronic Myeloid Leukemia Monitoring and Management.The oncologist · 2016Review
- New Developments in Chronic Myeloid Leukemia: Implications for Therapy.Iranian journal of cancer prevention · 2016Review
- Disruption of IKAROS activity in primitive chronic-phase CML cells mimics myeloid disease progression.Blood · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
The BCR-ABL1 oncogenic tyrosine kinase can transform pluripotent hematopoietic stem cells and initiate chronic myeloid leukemia in chronic phase (CML-CP), a myeloproliferative disorder characterized by excessive accumulation of mature myeloid cells. Patients in CML-CP usually respond to treatment with ABL1 tyrosine kinase inhibitors (TKIs) such as imatinib, though some patients who respond initially may become resistant later. CML-CP leukemia stem cells (LSCs) are intrinsically insensitive to TKIs and thus survive in the long term. These LSCs or their progeny may at some stage acquire additional genetic changes that cause the leukemia to transform further, from CML-CP to a more advanced phase, which has been subclassified as either accelerated phase (CML-AP) or blastic phase (CML-BP). CML-BP is characterized by a major clonal expansion of immature progenitors, which have either myeloid or lymphoid features. CML-BP responds poorly to treatment and is usually fatal. This review discusses the role of genomic instability leading to blastic transformation of CML and proposes some novel therapeutic approaches.
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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.