Fusion tyrosine kinases induce drug resistance by stimulation of homology-dependent recombination repair, prolongation of G(2)/M phase, and protection from apoptosis.
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JAK2 phosphorylates histone H3Y41 and excludes HP1alpha from chromatinUp-regulation of WRN and DNA ligase IIIalpha in chronic myeloid leukemia: consequences for the repair of DNA double-strand breaksEnhanced phosphorylation of Nbs1, a member of DNA repair/checkpoint complex Mre11-RAD50-Nbs1, can be targeted to increase the efficacy of imatinib mesylate against BCR/ABL-positive leukemia cellsCross talk of tyrosine kinases with the DNA damage signaling pathwaysTargeting DNA damage response in cancer therapyThe consequences of Rad51 overexpression for normal and tumor cellsTargeting RAD51 phosphotyrosine-315 to prevent unfaithful recombination repair in BCR-ABL1 leukemia.Phosphatidylinositol 3-kinase p85{alpha} subunit-dependent interaction with BCR/ABL-related fusion tyrosine kinases: molecular mechanisms and biological consequences.BCR-ABL1 kinase inhibits uracil DNA glycosylase UNG2 to enhance oxidative DNA damage and stimulate genomic instability.Functional screening identifies CRLF2 in precursor B-cell acute lymphoblastic leukemia.BCR-ABL stimulates mutagenic homologous DNA double-strand break repair via the DNA-end-processing factor CtIP.BCR/ABL modifies the kinetics and fidelity of DNA double-strand breaks repair in hematopoietic cells.Regulation of Rad51 promoter.Adenoviral vector driven by a minimal Rad51 promoter is selective for p53-deficient tumor cells.Targeting abnormal DNA double-strand break repair in tyrosine kinase inhibitor-resistant chronic myeloid leukemias.Cytostatic and cytotoxic effects of tyrphostin AG1296 on RMS cellsBCR/ABL regulates response to DNA damage: the role in resistance to genotoxic treatment and in genomic instability.Crosstalk between translesion synthesis, Fanconi anemia network, and homologous recombination repair pathways in interstrand DNA crosslink repair and development of chemoresistanceReactive Oxygen Species and Mitochondrial DNA Damage and Repair in BCR-ABL1 Cells Resistant to Imatinib.UV Differentially Induces Oxidative Stress, DNA Damage and Apoptosis in BCR-ABL1-Positive Cells Sensitive and Resistant to Imatinib.What have we learnt from mouse models of NPM-ALK-induced lymphomagenesis?Anaplastic lymphoma kinase and its signalling molecules as novel targets in lymphoma therapy.Polymorphism within the distal RAD51 gene promoter is associated with colorectal cancer in a Polish population.DNA Repair--A Double-Edged Sword in the Genomic Stability of Cancer Cells--The Case of Chronic Myeloid Leukemia.Fusion tyrosine kinase mediated signalling pathways in the transformation of haematopoietic cells.Tyrosine kinase inhibitor AG1024 exerts antileukaemic effects on STI571-resistant Bcr-Abl expressing cells and decreases AKT phosphorylation.BCR/ABL and other kinases from chronic myeloproliferative disorders stimulate single-strand annealing, an unfaithful DNA double-strand break repair.Clinical relevance of the homologous recombination machinery in cancer therapy.Use of the Rad51 promoter for targeted anti-cancer therapyLoss of the xeroderma pigmentosum group B protein binding site impairs p210 BCR/ABL1 leukemogenic activity.DNA repair by homologous recombination, but not by nonhomologous end joining, is elevated in breast cancer cells.Direct interaction of Ikaros and Foxp1 modulates expression of the G protein-coupled receptor G2A in B-lymphocytes and acute lymphoblastic leukemia.BCR-ABL: a multi-faceted promoter of DNA mutation in chronic myelogeneous leukemia.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.Targeting DNA repair and the cell cycle in glioblastoma.DNA repair and cytotoxic drugs: the potential role of RAD51 in clinical outcome of non-small-cell lung cancer patients.DNA double-strand break repair as determinant of cellular radiosensitivity to killing and target in radiation therapy.Potential mechanisms of disease progression and management of advanced-phase chronic myeloid leukemia.How should we define STAT3 as an oncogene and as a potential target for therapy?Oxidative metabolism in cancer: A STAT affair?
P2860
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P2860
Fusion tyrosine kinases induce drug resistance by stimulation of homology-dependent recombination repair, prolongation of G(2)/M phase, and protection from apoptosis.
description
2002 nî lūn-bûn
@nan
2002 թուականի Յունիսին հրատարակուած գիտական յօդուած
@hyw
2002 թվականի հունիսին հրատարակված գիտական հոդված
@hy
2002年の論文
@ja
2002年論文
@yue
2002年論文
@zh-hant
2002年論文
@zh-hk
2002年論文
@zh-mo
2002年論文
@zh-tw
2002年论文
@wuu
name
Fusion tyrosine kinases induce ...... and protection from apoptosis.
@ast
Fusion tyrosine kinases induce ...... and protection from apoptosis.
@en
Fusion tyrosine kinases induce ...... and protection from apoptosis.
@nl
type
label
Fusion tyrosine kinases induce ...... and protection from apoptosis.
@ast
Fusion tyrosine kinases induce ...... and protection from apoptosis.
@en
Fusion tyrosine kinases induce ...... and protection from apoptosis.
@nl
prefLabel
Fusion tyrosine kinases induce ...... and protection from apoptosis.
@ast
Fusion tyrosine kinases induce ...... and protection from apoptosis.
@en
Fusion tyrosine kinases induce ...... and protection from apoptosis.
@nl
P2093
P2860
P1476
Fusion tyrosine kinases induce ...... and protection from apoptosis.
@en
P2093
Artur Slupianek
Grazyna Hoser
Ireneusz Majsterek
Janusz Blasiak
Maciej Malecki
Richard Fishel
Tomasz Skorski
P2860
P304
P356
10.1128/MCB.22.12.4189-4201.2002
P407
P577
2002-06-01T00:00:00Z