Pardanani A, Elliott M, Reeder T, Li C Y, Baxter E J, Cross N C P, Tefferi A
Division of Hematology, Mayo Clinic, 200 First Street SW, Rochester, MN, USA.
Lancet. 2003 Aug 16;362(9383):535-6. doi: 10.1016/s0140-6736(03)14115-3.
Imatinib has shown to be effective against malignant disease driven by ckit. We prospectively treated 12 adults with symptomatic systemic mast-cell disease at a dose of either 100 mg or 400 mg per day. Of the ten patients who we could assess for response, five (50%) had a measurable response to the drug, four of whom had important mast-cell cytoreduction and two who had complete clinical and histological remission. In the five patients with eosinophilia, three had complete clinical and haematological remission. The other two, who did not respond to treatment, were the only patients with the ckit D816V mutation. Our results suggest that imatinib either inhibits the growth-promoting role of wild type ckit, or targets an oncogenic kinase.
伊马替尼已被证明对由c-kit驱动的恶性疾病有效。我们前瞻性地以每天100毫克或400毫克的剂量治疗了12名有症状的成人系统性肥大细胞病患者。在我们能够评估反应的10名患者中,5名(50%)对该药有可测量的反应,其中4名有显著的肥大细胞数量减少,2名有完全的临床和组织学缓解。在5名嗜酸性粒细胞增多的患者中,3名有完全的临床和血液学缓解。另外两名对治疗无反应的患者是仅有的携带c-kit D816V突变的患者。我们的结果表明,伊马替尼要么抑制野生型c-kit的促生长作用,要么靶向一种致癌激酶。