Genomic instability may originate from imatinib-refractory chronic myeloid leukemia stem cells.
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ZNF423 and ZNF521: EBF1 Antagonists of Potential Relevance in B-Lymphoid MalignanciesKinase-independent mechanisms of resistance of leukemia stem cells to tyrosine kinase inhibitorsPersonalized synthetic lethality induced by targeting RAD52 in leukemias identified by gene mutation and expression profile.ATRA-induced cellular differentiation and CD38 expression inhibits acquisition of BCR-ABL mutations for CML acquired resistanceCBP/catenin antagonist safely eliminates drug-resistant leukemia-initiating cells.Combined Population Dynamics and Entropy Modelling Supports Patient Stratification in Chronic Myeloid LeukemiaThe choice of first-line chronic myelogenous leukemia treatment.Clonal Evolution and Blast Crisis Correlate with Enhanced Proteolytic Activity of Separase in BCR-ABL b3a2 Fusion Type CML under Imatinib TherapyA novel mouse model identifies cooperating mutations and therapeutic targets critical for chronic myeloid leukemia progression.UV Differentially Induces Oxidative Stress, DNA Damage and Apoptosis in BCR-ABL1-Positive Cells Sensitive and Resistant to Imatinib.c-MYB is a transcriptional regulator of ESPL1/Separase in BCR-ABL-positive chronic myeloid leukemiaNormal ABL1 is a tumor suppressor and therapeutic target in human and mouse leukemias expressing oncogenic ABL1 kinases.Cooperation of imipramine blue and tyrosine kinase blockade demonstrates activity against chronic myeloid leukemia.Preclinical approaches in chronic myeloid leukemia: from cells to systemsKinase-inhibitor-insensitive cancer stem cells in chronic myeloid leukemia.Genetic events other than BCR-ABL1.Do we need more drugs for chronic myeloid leukemia?Nanocarrier-mediated drugs targeting cancer stem cells: an emerging delivery approach.Therapeutic potential of cancer stem cells.BCR-ABL1-positive microvesicles malignantly transform human bone marrow mesenchymal stem cells in vitro.Loss of mutL homolog-1 (MLH1) expression promotes acquisition of oncogenic and inhibitor-resistant point mutations in tyrosine kinases.Cellular and Molecular Networks in Chronic Myeloid Leukemia: The Leukemic Stem, Progenitor and Stromal Cell Interplay.Chaetocin antileukemia activity against chronic myelogenous leukemia cells is potentiated by bone marrow stromal factors and overcomes innate imatinib resistance.A 'telomere-associated secretory phenotype' cooperates with BCR-ABL to drive malignant proliferation of leukemic cells.CBP/Catenin antagonists: Targeting LSCs' Achilles heel.Anti-oxidant vitamin E prevents accumulation of imatinib-resistant BCR-ABL1 kinase mutations in CML-CP xenografts in NSG mice.Cytogenetic landscape and impact in blast phase of chronic myeloid leukemia in the era of tyrosine kinase inhibitor therapy.Mtss1 is a critical epigenetically regulated tumor suppressor in CML.Gene expression and mutation-guided synthetic lethality eradicates proliferating and quiescent leukemia cells.AKT-induced reactive oxygen species generate imatinib-resistant clones emerging from chronic myeloid leukemia progenitor cells.Disruption of IKAROS activity in primitive chronic-phase CML cells mimics myeloid disease progression.Role of NOX2 for leukaemic expansion in a murine model of BCR-ABL1(+) leukaemia.BCR-ABL1-positive microvesicles transform normal hematopoietic transplants through genomic instability: implications for donor cell leukemia.Targeting BCR-ABL-Independent TKI Resistance in Chronic Myeloid Leukemia by mTOR and Autophagy Inhibition.Genotoxicity associated with the use of tyrosine kinase inhibitors in patients with chronic myeloid leukemia.Auto-Commentary on: "Targeting mitochondrial oxidative phosphorylation eradicates therapy-resistant chronic myeloid leukemia stem cells".IGH/MYC Translocation Associates with BRCA2 Deficiency and Synthetic Lethality to PARP1 Inhibitors.Prospective analysis of low-level BCR-ABL1 T315I mutation in CD34 + cells of patients with de novo chronic myeloid leukemia.Tyrosine kinase inhibitor-induced defects in DNA repair sensitize FLT3(ITD)-positive leukemia cells to PARP1 inhibitors.Evaluation of the primitive fraction by functional in vitro assays at the RNA and DNA level represents a novel tool for complementing molecular monitoring in chronic myeloid leukemia.
P2860
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P2860
Genomic instability may originate from imatinib-refractory chronic myeloid leukemia stem cells.
description
2013 nî lūn-bûn
@nan
2013年の論文
@ja
2013年論文
@yue
2013年論文
@zh-hant
2013年論文
@zh-hk
2013年論文
@zh-mo
2013年論文
@zh-tw
2013年论文
@wuu
2013年论文
@zh
2013年论文
@zh-cn
name
Genomic instability may origin ...... c myeloid leukemia stem cells.
@en
type
label
Genomic instability may origin ...... c myeloid leukemia stem cells.
@en
prefLabel
Genomic instability may origin ...... c myeloid leukemia stem cells.
@en
P2093
P2860
P50
P1433
P1476
Genomic instability may origin ...... c myeloid leukemia stem cells.
@en
P2093
Elisabeth Bolton-Gillespie
Hardik Modi
Ilona Seferynska
Jacqueline Maier
Linda Kerstiens
Margaret Nieborowska-Skorska
Martin C Müller
Mateusz Koptyra
Mirle Schemionek
Ravi Bhatia
P2860
P304
P356
10.1182/BLOOD-2012-11-466938
P407
P50
P577
2013-03-29T00:00:00Z