ReviewFrontiers in genetics2021
A Review on the Therapeutic Role of TKIs in Case of CML in Combination With Epigenetic Drugs.
Review in Frontiers in genetics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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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.
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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.
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Who cites it
16 citing papers in PubMed, 27 citations in OpenAlex.
- Experimental Validation and Computational Deconstruction of Downstream Mutations in MIR5195: Integrating Whole-Exome Sequencing, Structural Dynamics, and Molecular Docking to Decipher Transcriptional Reprogramming in CML.Cell biochemistry and biophysics · 2026Article
- Olverembatinib (HQP1351): a third-generation tyrosine kinase inhibitor in the treatment of hematologic and solid malignancies-a comprehensive review of clinical outcomes.Discover oncology · 2026Review
- Targeting Lysosomes for Enhanced Anti-Cancer Therapeutics and Immune Response.International journal of biological sciences · 2026Review
- Study of the association between HDAC8, SIRT1, and P53 gene expression with drug resistance in chronic myeloid leukemia patients.BMC cancer · 2025Article
- Neddylation status determines the therapeutic sensitivity of tyrosine kinase inhibitors in chronic myeloid leukemia.Scientific reports · 2025Article
- Different In Vitro Models of Chronic Myeloid Leukemia Show Different Characteristics: Biological Replicates Are Not Biologically Equivalent.Cell biology international · 2025Article
- CD133-Guided RNA Nanoparticle Delivery of FTO siRNA Impairs Leukemia Resistance to Tyrosine Kinase Inhibitor Therapy.RNA nanomed · 2025Article
- AZ-628 sensitizes donafenib in hepatocellular carcinoma by targeting tyrosine kinase pathway and ferroptosis.CytoJournal · 2025Article
- The role of the lysine histone methylase KMT2D in chronic myeloid leukemia.Frontiers in pharmacology · 2025Article
- Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitors in Cancer: Current Use and Future Prospects.International journal of molecular sciences · 2024Review
- The mGenes & diseases · 2024Article
- Clinical applications of abnormal DNA methylation in chronic myeloid leukemia.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2024Article
- Hypertension in Cardio-Oncology Clinic: an update on etiology, assessment, and management.Cardio-oncology (London, England) · 2023Review
- Bullous Pemphigoid Occurring after Stopping Imatinib Therapy of CML: Is a Continuation of Post-Treatment Follow-Up Needed?Clinics and practice · 2023Article
- Growth Inhibitory and Pro-Apoptotic Effects of Hirsuteine in Chronic Myeloid Leukemia Cells through Targeting Sphingosine Kinase 1.Biomolecules & therapeutics · 2022Article
- Sporadic Medullary Thyroid Carcinoma: Towards a Precision Medicine.Frontiers in endocrinology · 2022Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic myeloid leukemia is a malignancy of bone marrow that affects white blood cells. There is strong evidence that disease progression, treatment responses, and overall clinical outcomes of CML patients are influenced by the accumulation of other genetic and epigenetic abnormalities, rather than only the BCR/ABL1 oncoprotein. Both genetic and epigenetic factors influence the efficacy of CML treatment strategies. Targeted medicines known as tyrosine-kinase inhibitors have dramatically improved long-term survival rates in CML patients during the previous 2 decades. When compared to earlier chemotherapy treatments, these drugs have revolutionized CML treatment and allowed most people to live longer lives. Although epigenetic inhibitors' activity is disrupted in many cancers, including CML, but when combined with TKI, they may offer potential therapeutic strategies for the treatment of CML cells. The epigenetics of tyrosine kinase inhibitors and resistance to them is being studied, with a particular focus on imatinib, which is used to treat CML. In addition, the use of epigenetic drugs in conjunction with TKIs has been discussed. Resistance to TKIs is still a problem in curing the disease, necessitating the development of new therapies. This study focused on epigenetic pathways involved in CML pathogenesis and tumor cell resistance to TKIs, both of which contribute to leukemic clone breakout and proliferation.
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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.