Excess of NPM-ALK oncogenic signaling promotes cellular apoptosis and drug dependency

No abstract is available for this paper.

• Publication year

  2015

• Venue

  Oncogene

• Publication date

  2015-12-14

• Fields of study

  Biology, Medicine

• Identifiers
  DOI 10.1038/onc.2015.456PMID 26657151PMCID PMC4907875
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

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  2014cited by this paper
• DNA replication and oncogene-induced replicative stress.

  2014cited by this paper
• Ceritinib in ALK-rearranged non-small-cell lung cancer.

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• Activating mutations in ALK kinase domain confer resistance to structurally unrelated ALK inhibitors in NPM-ALK-positive anaplastic large-cell lymphoma

  2014cited by this paper
• Two Novel ALK Mutations Mediate Acquired Resistance to the Next-Generation ALK Inhibitor Alectinib

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• Reversible and adaptive resistance to BRAF(V600E) inhibition in melanoma

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• Myc and Ras oncogenes engage different energy metabolism programs and evoke distinct patterns of oxidative and DNA replication stress

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• Crizotinib in advanced, chemoresistant anaplastic lymphoma kinase-positive lymphoma patients.

  2014cited by this paper
• Ceritinib in ALK-rearranged non-small-cell lung cancer.

  2014cited by this paper
• Treatment Efficacy and Resistance Mechanisms Using the Second-Generation ALK Inhibitor AP26113 in Human NPM-ALK–Positive Anaplastic Large Cell Lymphoma

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• The ALK inhibitor ceritinib overcomes crizotinib resistance in non-small cell lung cancer.

  2014cited by this paper
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• Mechanisms of Acquired Crizotinib Resistance in ALK-Rearranged Lung Cancers

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• KPT‐330 inhibitor of CRM1 (XPO1)‐mediated nuclear export has selective anti‐leukaemic activity in preclinical models of T‐cell acute lymphoblastic leukaemia and acute myeloid leukaemia

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• Modelling vemurafenib resistance in melanoma reveals a strategy to forestall drug resistance

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• Mechanistic insight into ALK receptor tyrosine kinase in human cancer biology

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  2009cited by this paper
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• An Oncogene-Induced DNA Damage Model for Cancer Development

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• The tyrosine phosphatase Shp2 interacts with NPM-ALK and regulates anaplastic lymphoma cell growth and migration.

  2007cited by this paper
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• Ablation of oncogenic ALK is a viable therapeutic approach for anaplastic large-cell lymphomas.

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• p53 gene mutations are uncommon but p53 is commonly expressed in anaplastic large-cell lymphoma

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• Clinical Resistance to STI-571 Cancer Therapy Caused by BCR-ABL Gene Mutation or Amplification

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• Transcriptional activation by tetracyclines in mammalian cells.

  1995cited by this paper
• Fusion of a kinase gene, ALK, to a nucleolar protein gene, NPM, in non-Hodgkin's lymphoma.

  1994cited by this paper
• Fusion of a kinase gene, ALK, to a nucleolar protein gene, NPM, in non-Hodgkin's lymphoma.

  1994cited by this paper

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• Nuclear NPM-ALK Protects Myc from Proteasomal Degradation and Contributes to Its High Expression in Cancer Stem-Like Cells in ALK-Positive Anaplastic Large Cell Lymphoma

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