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10.1097/MOH.0000000000000256

http://scihub22266oqcxt.onion/10.1097/MOH.0000000000000256
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C5112586!5112586!27101528
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suck abstract from ncbi


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pmid27101528      Curr+Opin+Hematol 2016 ; 23 (4): 416-25
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  • Histiocytic Neoplasms in the Era of Personalized Genomic Medicine #MMPMID27101528
  • Durham BH; Diamond EL; Abdel-Wahab O
  • Curr Opin Hematol 2016[Jul]; 23 (4): 416-25 PMID27101528show ga
  • Purpose of Review: Since the discovery of BRAFV600E mutations in histiocytic neoplasms, diverse kinase alterations have been uncovered in BRAFV600E-wildtype histiocytoses. The purpose of this review is to outline recent molecular advances in histiocytic neoplasms and discuss their impact on the pathogenesis and treatment of these disorders. Recent Findings: Activating kinase alterations discovered in BRAFV600E-wildtype Langerhans (LCH) and non-Langerhans cell histiocytoses (non-LCH) result in constitutive activation of the mitogen-activated protein kinase (MAPK) and/or PI3K/AKT pathways. These kinase alterations include activating mutations in ARAF, MAP2K1, NRAS, KRAS, and PIK3CA kinases in LCH and non-LCH; BRAF, ALK, and NTRK1 fusions, as well as the ETV3-NCOA2 fusion in non-LCH; and mutations in the MAP3K1 and HRAS kinases in LCH and histiocytic sarcoma, respectively. These discoveries have refined the understanding of the histiocytoses as clonal, myeloid neoplasms driven by constitutive MAPK signaling and identified molecular therapeutic targets with promising clinical responses to RAF and MEK inhibition. Summary: Genomic analyses over the last 6 years have identified targetable kinase alterations in BRAFV600E-wildtype histiocytic neoplasms. However, despite this progress, the molecular pathogenesis and therapeutic responsiveness of non-BRAFV600E kinase alterations are still poorly defined in these disorders.
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