BRAF in non-small cell lung cancer (NSCLC): Pickaxing another brick in the wall
作者: Alessandro LeonettiFrancesco FacchinettiGiulio RossiRoberta MinariAntonia ContiLuc FribouletMarcello TiseoDavid Planchard
作者单位: 1Medical Oncology Unit, University Hospital of Parma, Parma, Italy
2Pathology Unit, Santa Maria delle Croci Hospital, Ravenna, Italy
3Medical Illustrator, Riccione, Italy
4INSERM, U981, Gustave Roussy Cancer Campus, Villejuif, France
5Department of Medical Oncology, Gustave Roussy Cancer Campus, Villejuif, France
刊名: Cancer Treatment Reviews, 2018, Vol.66 , pp.82-94
来源数据库: Elsevier Journal
DOI: 10.1016/j.ctrv.2018.04.006
关键词: Non-small cell lung cancer (NSCLC)BRAF mutationsMitogen activated protein kinase (MAPK)/extracellular signal-regulated kinase (ERK) pathwayVemurafenibDabrafenibTrametinib
英文摘要: Abstract(#br)Molecular characterization of non-small cell lung cancer (NSCLC) marked an historical turning point for the treatment of lung tumors harboring kinase alterations suitable for specific targeted drugs inhibition, translating into major clinical improvements. Besides EGFR, ALK and ROS1, BRAF represents a novel therapeutic target for the treatment of advanced NSCLC. BRAF mutations, found in 1.5–3.5% of NSCLC, are responsible of the constitutive activation of mitogen activated protein kinase (MAPK)/extracellular signal-regulated kinase (ERK) pathway. Clinical trials evaluating the efficacy of the BRAF inhibitor dabrafenib in combination with the downstream MEK inhibitor trametinib in metastatic BRAF V600E -mutated NSCLC guaranteed FDA and EMA rapid approval of the combination...
全文获取路径: Elsevier  (合作)
影响因子:6.024 (2012)

  • cancer 癌症
  • kinase 激酶
  • regulated 规定
  • protein 蛋白质
  • brick 
  • pathway 轨道
  • activated 激化了的
  • small 小的
  • extracellular 胞外的
  • another 别的