ReviewOncogene2002
BCR/ABL regulates response to DNA damage: the role in resistance to genotoxic treatment and in genomic instability.
Review in Oncogene, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
What it found
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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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Who cites it
40 citing papers in PubMed, 136 citations in OpenAlex.
- Molecular mechanisms of circadian clock-mediated gene regulation and their implications in leukemia.Molecular biology reports · 2026Review
- DNA polymerase kappa stabilized by Ptbp2 interacts with MRE11 and promotes genomic instability in leukemia.Cell death discovery · 2026Article
- Styrylquinazoline derivatives as ABL inhibitors selective for different DFG orientations.Journal of enzyme inhibition and medicinal chemistry · 2023Article
- Targeting MDC1 promotes apoptosis and sensitizes Imatinib resistance in CML cells by mainly disrupting non-homologous end-joining repair.Medical oncology (Northwood, London, England) · 2022Article
- ASXL1 mutations predict inferior molecular response to nilotinib treatment in chronic myeloid leukemia.Leukemia · 2022Article
- Proteolysis-targeting chimeras (PROTACs) in cancer therapy.Molecular cancer · 2022Review
- Review
- Oxidative Stress in Cancer Cell Metabolism.Antioxidants (Basel, Switzerland) · 2021Review
- Tyrosine kinase c-Abl couples RNA polymerase II transcription to DNA double-strand breaks.Nucleic acids research · 2019Article
- Targeting WEE1 to enhance conventional therapies for acute lymphoblastic leukemia.Journal of hematology & oncology · 2018Article
- FusionPathway: Prediction of pathways and therapeutic targets associated with gene fusions in cancer.PLoS computational biology · 2018Article
- Chronic exposure to low dose of bisphenol A impacts on the first round of spermatogenesis via SIRT1 modulation.Scientific reports · 2018Article
- Article
- Modeling the influence of stromal microenvironment in the selection of ENU-induced BCR-ABL1 mutants by tyrosine kinase inhibitors.Oncoscience · 2014Article
- ETV6/RUNX1 induces reactive oxygen species and drives the accumulation of DNA damage in B cells.Neoplasia (New York, N.Y.) · 2013Article
- Targeting abnormal DNA double-strand break repair in tyrosine kinase inhibitor-resistant chronic myeloid leukemias.Oncogene · 2013Article
- DNA double-strand break repair as determinant of cellular radiosensitivity to killing and target in radiation therapy.Frontiers in oncology · 2013Article
- Identification of nuclear protein targets for six leukemogenic tyrosine kinases governed by post-translational regulation.PloS one · 2012Article
- Article
- Antitumor effect of betulinic acid on human acute leukemia K562 cells in vitro.Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban · 2010Article
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
No grant is acknowledged in the PubMed record.
Abstract
BCR/ABL regulates cell proliferation, apoptosis, differentiation and adhesion. In addition, BCR/ABL can induce resistance to cytostatic drugs and irradiation by modulation of DNA repair mechanisms, cell cycle checkpoints and Bcl-2 protein family members. Upon DNA damage BCR/ABL not only enhances reparation of DNA lesions (e.g. homologous recombination repair), but also prolongs activation of cell cycle checkpoints (e.g. G2/M) providing more time for repair of otherwise lethal lesions. Moreover, by modification of anti-apoptotic members of the Bcl-2 family (e.g. upregulation of Bcl-x(L)) BCR/ABL provides a cytoplasmic 'umbrella' protecting mitochondria from the 'rain' of apoptotic signals coming from the damaged DNA in the nucleus, thus preventing release of cytochrome c and activation of caspases. The unrepaired and/or aberrantly repaired (but not lethal) DNA lesions resulting from spontaneous and/or drug-induced damage can accumulate in BCR/ABL-transformed cells leading to genomic instability and malignant progression of the disease. Inhibition of BCR/ABL kinase activity by STI571 (Gleevec, imatinib mesylate) reverses drug resistance and, in combination with standard chemotherapeutics can exert strong anti-leukemia effect.
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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.