ReviewLeukemia & lymphoma2011
Chronic myeloid leukemia cells refractory/resistant to tyrosine kinase inhibitors are genetically unstable and may cause relapse and malignant progression to the terminal disease state.
Review in Leukemia & lymphoma, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
20 citing papers in PubMed, 37 citations in OpenAlex.
- Review
- Genetic Biomarkers in Chronic Myeloid Leukemia: What Have We Learned So Far?International journal of molecular sciences · 2021Review
- Resistance to Tyrosine Kinase Inhibitors in Chronic Myeloid Leukemia-From Molecular Mechanisms to Clinical Relevance.Cancers · 2021Review
- Potential ApproachesFrontiers in oncology · 2021Review
- Understanding and Monitoring Chronic Myeloid Leukemia Blast Crisis: How to Better Manage Patients.Cancer management and research · 2021Review
- Article
- Article
- Chronic myelogenous leukemia, a still unsolved problem: pitfalls and new therapeutic possibilities.Drug design, development and therapy · 2019Review
- Genomic instability is a principle pathologic feature of FLT3 ITD kinase activity in acute myeloid leukemia leading to clonal evolution and disease progression.Leukemia & lymphoma · 2017Review
- Cellular and Molecular Networks in Chronic Myeloid Leukemia: The Leukemic Stem, Progenitor and Stromal Cell Interplay.Current drug targets · 2017Review
- The role of dasatinib in the management of chronic myeloid leukemia.Drug design, development and therapy · 2015Review
- Radiopharmaceutical therapy in the era of precision medicine.European journal of cancer (Oxford, England : 1990) · 2014Article
- BMI1 reprogrammes histone acetylation and enhances c-fos pathway via directly binding to Zmym3 in malignant myeloid progression.Journal of cellular and molecular medicine · 2014Article
- Dosimetry for radiopharmaceutical therapy.Seminars in nuclear medicine · 2014Review
- ETV6/RUNX1 induces reactive oxygen species and drives the accumulation of DNA damage in B cells.Neoplasia (New York, N.Y.) · 2013Article
- BCR-ABL1 kinase inhibits uracil DNA glycosylase UNG2 to enhance oxidative DNA damage and stimulate genomic instability.Leukemia · 2013Article
- Human induced pluripotent stem cells from basic research to potential clinical applications in cancer.BioMed research international · 2013Review
- The bone marrow microenvironment as niche retreats for hematopoietic and leukemic stem cells.Advances in hematology · 2013Article
- Chronic myeloid leukemia 2011: successes, challenges, and strategies--proceedings of the 5th annual BCR-ABL1 positive and BCR-ABL1 negative myeloproliferative neoplasms workshop.American journal of hematology · 2011Article
- Involvement of Oxidative Stress in Resistance to Tyrosine-Kinase Inhibitors Therapy in Chronic Myeloid Leukemia.Current health sciences journalArticle
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
BCR-ABL1 kinase-induced chronic myeloid leukemia in chronic phase (CML-CP) usually responds to treatment with ABL tyrosine kinase inhibitors (TKIs) such as imatinib, dasatinib, and nilotinib. In most patients TKIs reduce the leukemia cell load substantially, but some leukemia cells, for example leukemia stem cells (LSCs), are intrinsically refractory to TKIs. In addition, some patients who respond initially may later become resistant to TKIs due to accumulation of point mutations in BCR-ABL1 kinase. LSCs or their progeny, leukemia progenitor cells (LPCs), at some stage may acquire additional genetic changes that cause the leukemia to transform further to a more advanced blast phase (CML-BP), which responds poorly to treatment and is usually fatal. We postulate that LSCs and/or LPCs refractory or resistant to TKIs may be 'ticking time-bombs' accumulating additional genetic aberrations and eventually 'exploding' to generate additional TKI-resistant clones and CML-BP clones with complex karyotypes.
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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.