UV Differentially Induces Oxidative Stress, DNA Damage and Apoptosis in BCR-ABL1-Positive Cells Sensitive and Resistant to Imatinib
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Summary
Imatinib-resistant cells may display a different extent of genome instability than their imatinIB-sensitive counterparts, which may follow their different reactions to both endogenous and exogenous DNA-damaging factors, including DNA repair and apoptosis.
- Type
- article
- Published
- 2015-08-01
- Cited by
- 19
- References
- 41
- Access
- Open access
- OpenAlex
- https://openalex.org/W2111911815
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:11201366
Keywords
Oxidative stress, DNA damage, Apoptosis, Imatinib, breakpoint cluster region
References
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- Seeking the causes and solutions to imatinib-resistance in chronic myeloid leukemia
- ATRA-Induced Cellular Differentiation and CD38 Expression Inhibits Acquisition of BCR-ABL Mutations for CML Acquired Resistance
- UVA-induced cyclobutane pyrimidine dimers in DNA: a direct photochemical mechanism?
- BCR-ABL1 kinase inhibits uracil DNA glycosylase UNG2 to enhance oxidative DNA damage and stimulate genomic instability
- Use of Second- and Third-Generation Tyrosine Kinase Inhibitors in the Treatment of Chronic Myeloid Leukemia: An Evolving Treatment Paradigm
- Overproduction of BCR‐ABL induces apoptosis in imatinib mesylate‐resistant cell lines
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- STI571 reduces NER activity in BCR/ABL-expressing cells.
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- Current aspects in resistance against tyrosine kinase inhibitors in chronic myelogenous leukemia.
- BCR/ABL, DNA damage and DNA repair: Implications for new treatment concepts
- Mitochondrial membrane potential regulates matrix configuration and cytochrome c release during apoptosis
- Induction of bystander effects by UVA, UVB, and UVC radiation in human fibroblasts and the implication of reactive oxygen species.
- XPC genetic polymorphisms correlate with the response to imatinib treatment in patients with chronic phase chronic myeloid leukemia
Cited by
- Doxorubicin Differentially Induces Apoptosis, Expression of Mitochondrial Apoptosis-Related Genes, and Mitochondrial Potential in BCR-ABL1-Expressing Cells Sensitive and Resistant to Imatinib
- Mitochondrial mutagenesis in BCR-ABL1-expressing cells sensitive and resistant to imatinib.
- A Protective Mechanism of Visible Red Light in Normal Human Dermal Fibroblasts: Enhancement of GADD45A-Mediated DNA Repair Activity.
- An exploratory study by DMET array identifies a germline signature associated with imatinib response in gastrointestinal stromal tumor
- Highly Crystalline WO3 Nanoparticles Are Nontoxic to Stem Cells and Cancer Cells
- Relationship of oxidative stress in the resistance to imatinib in Tunisian patients with chronic myeloid leukemia: A retrospective study
- Jujube and green tea extracts protect human fibroblast cells against UVB-mediated photo damage and MMP-2 and MMP-9 production
- Melittin—A Natural Peptide from Bee Venom Which Induces Apoptosis in Human Leukaemia Cells
- [Effect of ultraviolet irradiation on the proliferation of acute promyelocytic leukemia cells under hypoxic conditions and related mechanisms].
- Pharmacogenetics in the treatment of gastrointestinal stromal tumors – an updated review
- Relationship between Oxidative Stress and Imatinib Resistance in Model Chronic Myeloid Leukemia Cells
- Protein disulfide isomerase family 6 promotes the imatinib-resistance of renal cell carcinoma by regulation of Wnt3a-Frizzled1 axis
- Ultraviolet Radiation Promoted Hypoxia-Induced Apoptosis in HL-60 Human Promyelocytic Leukemia Cell Line
- A Comprehensive Metabolism-Related Gene Signature Predicts the Survival of Patients with Acute Myeloid Leukemia
- Oxidative Stress and Chronic Myeloid Leukemia: A Balance between ROS-Mediated Pro- and Anti-Apoptotic Effects of Tyrosine Kinase Inhibitors
- K-562 Extracellular Vesicles Partially Protect Intact Cells from Oxidative Stress and Provide Limited Resistance to Imatinib
- Dose-specific lncRNA-mRNA networks modulate DNA damage and immune responses in CD4⁺ T cells under simulated space UVC irradiation.
- Targeting Mitochondrial Vulnerabilities in Chronic Myeloid Leukemia: From Pathobiology to Novel Therapeutic Opportunities
- Highly Crystalline WO 3 Nanoparticles Are Nontoxic to Stem Cells and Cancer Cells
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