What have we learnt from mouse models of NPM-ALK-induced lymphomagenesis?
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ALK Signaling and Target Therapy in Anaplastic Large Cell LymphomaAnaplastic lymphoma kinase: signalling in development and diseaseEvaluation of EML4-ALK fusion proteins in non-small cell lung cancer using small molecule inhibitorsInhibition of anaplastic lymphoma kinase (ALK) activity provides a therapeutic approach for CLTC-ALK-positive human diffuse large B cell lymphomas.Aberrant anaplastic lymphoma kinase activity induces a p53 and Rb-dependent senescence-like arrest in the absence of detectable p53 stabilizationA novel role for IL-22R1 as a driver of inflammation.Identification of NVP-TAE684, a potent, selective, and efficacious inhibitor of NPM-ALK.Inhibition of Rac controls NPM-ALK-dependent lymphoma development and disseminationAutocrine release of interleukin-9 promotes Jak3-dependent survival of ALK+ anaplastic large-cell lymphoma cells.ALK-immunoreactive neoplasms.Anaplastic large cell lymphoma arises in thymocytes and requires transient TCR expression for thymic egress.Assays for pharmacodynamic analysis of histone deacetylase inhibitors.Targeting autophagy enhances the anti-tumoral action of crizotinib in ALK-positive anaplastic large cell lymphoma.Nucleophosmin: a versatile molecule associated with hematological malignancies.The natural product avrainvillamide binds to the oncoprotein nucleophosmin.Anaplastic lymphoma kinase-positive large B-cell lymphoma: a distinct clinicopathological entityBeyond NPM-anaplastic lymphoma kinase driven lymphomagenesis: alternative drivers in anaplastic large cell lymphoma.ALK-positive cancer: still a growing entity.Determining the contribution of NPM1 heterozygosity to NPM-ALK-induced lymphomagenesis.Silibinin suppresses NPM-ALK, potently induces apoptosis and enhances chemosensitivity in ALK-positive anaplastic large cell lymphoma.Anaplastic large cell lymphoma-propagating cells are detectable by side population analysis and possess an expression profile reflective of a primitive origin.Assessment of the transforming potential of novel anaplastic lymphoma kinase point mutants.Challenging perspectives on the cellular origins of lymphoma.Arsenic trioxide degrades NPM-ALK fusion protein and inhibits growth of ALK-positive anaplastic large cell lymphoma.The pleiotrophin-ALK axis is required for tumorigenicity of glioblastoma stem cells.JSI-124 (cucurbitacin I) inhibits Janus kinase-3/signal transducer and activator of transcription-3 signalling, downregulates nucleophosmin-anaplastic lymphoma kinase (ALK), and induces apoptosis in ALK-positive anaplastic large cell lymphoma cells.Hypoxia-microRNA-16 downregulation induces VEGF expression in anaplastic lymphoma kinase (ALK)-positive anaplastic large-cell lymphomas.Mouse Model of Poorly Differentiated Thyroid Carcinoma Driven by STRN-ALK Fusion
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What have we learnt from mouse models of NPM-ALK-induced lymphomagenesis?
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2005 nî lūn-bûn
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2005年の論文
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2005年論文
@yue
2005年論文
@zh-hant
2005年論文
@zh-hk
2005年論文
@zh-mo
2005年論文
@zh-tw
2005年论文
@wuu
2005年论文
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2005年论文
@zh-cn
name
What have we learnt from mouse models of NPM-ALK-induced lymphomagenesis?
@ast
What have we learnt from mouse models of NPM-ALK-induced lymphomagenesis?
@en
type
label
What have we learnt from mouse models of NPM-ALK-induced lymphomagenesis?
@ast
What have we learnt from mouse models of NPM-ALK-induced lymphomagenesis?
@en
prefLabel
What have we learnt from mouse models of NPM-ALK-induced lymphomagenesis?
@ast
What have we learnt from mouse models of NPM-ALK-induced lymphomagenesis?
@en
P2860
P356
P1433
P1476
What have we learnt from mouse models of NPM-ALK-induced lymphomagenesis?
@en
P2093
Alexander DR
P2860
P2888
P304
P356
10.1038/SJ.LEU.2403797
P577
2005-07-01T00:00:00Z