Kasi Pashtoon M, Litzow Mark R, Patnaik Mrinal M, Hashmi Shahrukh K, Gangat Naseema
Division of Hematology, Mayo Clinic, Rochester, MN, United States.
Leuk Res Rep. 2016 Jan 12;5:7-10. doi: 10.1016/j.lrr.2016.01.002. eCollection 2016.
For acute myeloid leukemia (AML), identification of activating mutations in the FMS-like tyrosine kinase-3 (FLT3) has led to the development of several FLT3-inhibitors. Here we present clinical and next generation sequencing data at the time of progression of a patient on a novel FLT3-inhibitor clinical trial (ASP2215) to show that employing therapeutic interventions with these novel targeted therapies can lead to consequences secondary to selective pressure and clonal evolution of cancer. We describe novel findings alongside data on treatment directed towards actionable aberrations acquired during the process. (
NCT02014558; registered at: 〈https://clinicaltrials.gov/ct2/show/NCT02014558〉).
对于急性髓系白血病（AML），FMS样酪氨酸激酶3（FLT3）激活突变的鉴定促使了几种FLT3抑制剂的研发。在此，我们展示了一名患者在一项新型FLT3抑制剂临床试验（ASP2215）进展时的临床和二代测序数据，以表明采用这些新型靶向治疗的干预措施会导致癌症选择性压力和克隆进化的继发后果。我们描述了新发现以及针对在此过程中获得的可操作异常进行治疗的数据。（临床试验：NCT02014558；注册于：〈https://clinicaltrials.gov/ct2/show/NCT02014558〉）
