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10.1016/j.leukres.2013.12.027

http://scihub22266oqcxt.onion/10.1016/j.leukres.2013.12.027
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suck abstract from ncbi


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pmid24486291
      Leuk+Res 2014 ; 38 (4 ): 503-8
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  • Crizotinib (PF-2341066) induces apoptosis due to downregulation of pSTAT3 and BCL-2 family proteins in NPM-ALK(+) anaplastic large cell lymphoma #MMPMID24486291
  • Hamedani FS ; Cinar M ; Mo Z ; Cervania MA ; Amin HM ; Alkan S
  • Leuk Res 2014[Apr]; 38 (4 ): 503-8 PMID24486291 show ga
  • Nucleophosmin-anaplastic lymphoma kinase (NPM-ALK) is an aberrant fusion gene product with tyrosine kinase activity and is expressed in substantial subset of anaplastic large cell lymphomas (ALCL). It has been shown that NPM-ALK binds to and activates signal transducer and activator of transcription 3 (STAT3). Although NPM-ALK(+) ALCL overall shows a better prognosis, there is a sub-group of patients who relapses and is resistant to conventional chemotherapeutic regimens. NPM-ALK is a potential target for small molecule kinase inhibitors. Crizotinib (PF-2341066) is a small, orally bioavailable molecule that inhibits growth of tumors with ALK activity as shown in a subgroup of non-small lung cancer patients with EML4-ALK expression. In this study, we have investigated the in vitro effects of Crizotinib in ALCL cell line with NPM-ALK fusion. Crizotinib induced marked downregulation of STAT3 phosphorylation, which was associated with significant apoptotic cell death. Apoptosis induction was attributed to caspase-3 cleavage and marked downregulation of the Bcl-2 family of proteins including MCL-1. These findings implicate that Crizotinib has excellent potential to treat patients with NPM-ALK(+) ALCL through induction of apoptotic cell death and downregulation of major oncogenic proteins in this aggressive lymphoma.
  • |Apoptosis/*drug effects [MESH]
  • |Cell Proliferation/drug effects [MESH]
  • |Crizotinib [MESH]
  • |Down-Regulation/drug effects [MESH]
  • |Humans [MESH]
  • |Lymphoma, Large-Cell, Anaplastic/genetics/*metabolism [MESH]
  • |Phosphorylation [MESH]
  • |Protein Kinase Inhibitors/*pharmacology [MESH]
  • |Protein-Tyrosine Kinases/genetics/metabolism [MESH]
  • |Proto-Oncogene Proteins c-bcl-2/*metabolism [MESH]
  • |Pyrazoles/*pharmacology [MESH]
  • |Pyridines/*pharmacology [MESH]
  • |STAT3 Transcription Factor/*metabolism [MESH]


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