Nilotinib and MEK inhibitors induce synthetic lethality through paradoxical activation of RAF in drug-resistant chronic myeloid leukemia
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Oncogene Overdose: Too Much of a Bad Thing for Oncogene-Addicted Cancer CellsDrugging the unfolded protein response in acute leukemiasThe dynamic nature of the kinomeAbl Kinases Regulate HGF/Met Signaling Required for Epithelial Cell Scattering, Tubulogenesis and MotilityInhibitors that stabilize a closed RAF kinase domain conformation induce dimerizationRole of ABL family kinases in cancer: from leukaemia to solid tumoursIdentification of drug combinations containing imatinib for treatment of BCR-ABL+ leukemiasRegistered report: Kinase-dead BRAF and oncogenic RAS cooperate to drive tumor progression through CRAFA therapeutically targetable mechanism of BCR-ABL-independent imatinib resistance in chronic myeloid leukemia.Dasatinib worsens the effect of cetuximab in combination with fractionated radiotherapy in FaDu- and A431-derived xenografted tumoursParadoxical MAPK-activation in response to treatment with tyrosine kinase inhibitors in CML: flow cytometry loses track.MEK/ERK dependent activation of STAT1 mediates dasatinib-induced differentiation of acute myeloid leukemia.Spred2 modulates the erythroid differentiation induced by imatinib in chronic myeloid leukemia cellsRecent progress in targeting cancer.Complexity in the signaling network: insights from the use of targeted inhibitors in cancer therapy.Drug-induced RAF dimerization is independent of RAS mutation status and does not lead to universal MEK dependence for cell survival in head and neck cancersThe Emerging Role of ABL Kinases in Solid Tumors.Dasatinib induces DNA damage and activates DNA repair pathways leading to senescence in non-small cell lung cancer cell lines with kinase-inactivating BRAF mutationsA tale of two approaches: complementary mechanisms of cytotoxic and targeted therapy resistance may inform next-generation cancer treatmentsDeregulated hedgehog pathway signaling is inhibited by the smoothened antagonist LDE225 (Sonidegib) in chronic phase chronic myeloid leukaemiaCommon drugs and treatments for cancer and age-related diseases: revitalizing answers to NCI's provocative questions.Imatinib and Nilotinib increase glioblastoma cell invasion via Abl-independent stimulation of p130Cas and FAK signalling.ABL kinases promote breast cancer osteolytic metastasis by modulating tumor-bone interactions through TAZ and STAT5 signaling.Kinase-impaired BRAF mutations in lung cancer confer sensitivity to dasatinibCombined targeting of BCL-2 and BCR-ABL tyrosine kinase eradicates chronic myeloid leukemia stem cells.Inactivation of ABL kinases suppresses non-small cell lung cancer metastasis.Cross-talk between EphA2 and BRaf/CRaf is a key determinant of response to Dasatinib.Primary melanoma of the CNS in children is driven by congenital expression of oncogenic NRAS in melanocytes.Standardized definitions of molecular response in chronic myeloid leukemia.It takes two to tango--signalling by dimeric Raf kinases.Aggressive behavior and anaplasia in pleomorphic xanthoastrocytoma: a plea for a revision of the current WHO classification.Chronic myeloid leukemia: advances in understanding disease biology and mechanisms of resistance to tyrosine kinase inhibitors.Treatment inferred from mutations identified using massive parallel sequencing leads to clinical benefit in some heavily pretreated cancer patientsNatural course and biology of CML.Update on emerging treatments for chronic myeloid leukemia.Induction of immunoglobulin transcription factor 2 and resistance to MEK inhibitor in melanoma cells.Opportunities and challenges provided by crosstalk between signalling pathways in cancer.Quantitative phosphoproteomic analysis of acquired cancer drug resistance to pazopanib and dasatinib.The Mitogen-Activated Protein Kinase Pathway Facilitates Resistance to the Src Inhibitor Dasatinib in Thyroid Cancer.Proteomic strategy for probing complementary lethality of kinase inhibitors against pancreatic cancer.
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P2860
Nilotinib and MEK inhibitors induce synthetic lethality through paradoxical activation of RAF in drug-resistant chronic myeloid leukemia
description
2011 nî lūn-bûn
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2011 թուականի Դեկտեմբերին հրատարակուած գիտական յօդուած
@hyw
2011 թվականի դեկտեմբերին հրատարակված գիտական հոդված
@hy
2011年の論文
@ja
2011年論文
@yue
2011年論文
@zh-hant
2011年論文
@zh-hk
2011年論文
@zh-mo
2011年論文
@zh-tw
2011年论文
@wuu
name
Nilotinib and MEK inhibitors i ...... stant chronic myeloid leukemia
@ast
Nilotinib and MEK inhibitors i ...... stant chronic myeloid leukemia
@en
Nilotinib and MEK inhibitors i ...... stant chronic myeloid leukemia
@en-gb
Nilotinib and MEK inhibitors i ...... stant chronic myeloid leukemia
@nl
type
label
Nilotinib and MEK inhibitors i ...... stant chronic myeloid leukemia
@ast
Nilotinib and MEK inhibitors i ...... stant chronic myeloid leukemia
@en
Nilotinib and MEK inhibitors i ...... stant chronic myeloid leukemia
@en-gb
Nilotinib and MEK inhibitors i ...... stant chronic myeloid leukemia
@nl
prefLabel
Nilotinib and MEK inhibitors i ...... stant chronic myeloid leukemia
@ast
Nilotinib and MEK inhibitors i ...... stant chronic myeloid leukemia
@en
Nilotinib and MEK inhibitors i ...... stant chronic myeloid leukemia
@en-gb
Nilotinib and MEK inhibitors i ...... stant chronic myeloid leukemia
@nl
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P2860
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P3181
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Nilotinib and MEK inhibitors i ...... stant chronic myeloid leukemia
@en
P2093
Ana Rebocho
Christopher A Eide
Ion Niculescu-Duvaz
Leisl M Packer
Matthew S Zabriskie
Robert Hayward
Sareena Rana
Sonja Heidorn
Thomas O'Hare
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P304
P3181
P356
10.1016/J.CCR.2011.11.004
P407
P577
2011-12-13T00:00:00Z