Division of Hematology, Department of Medicine, Stanford University School of Medicine/Stanford Cancer Institute, Stanford, CA 94305-5821, USA.
Blood. 2013 Sep 5;122(10):1707-11. doi: 10.1182/blood-2013-05-500959. Epub 2013 Jul 29.
Although activation of tyrosine kinase pathways is a shared theme among myeloproliferative neoplasms, the pathogenetic basis of chronic neutrophilic leukemia (CNL) has remained elusive. Recently, we identified high-frequency oncogenic mutations in the granulocyte-colony stimulating factor receptor (CSF3R) in CNL and in some patients with atypical chronic myeloid leukemia. Inhibition of Janus kinase 2 or SRC kinase signaling downstream of mutated CSF3R is feasible and should be explored therapeutically. Herein, we discuss the potential impact of these findings for the classification and treatment of these disorders.
虽然酪氨酸激酶途径的激活是骨髓增殖性肿瘤的共同主题，但慢性中性粒细胞白血病（CNL）的发病机制仍不清楚。最近，我们在 CNL 和一些非典型慢性髓性白血病患者中发现了粒细胞集落刺激因子受体（CSF3R）的高频致癌突变。抑制突变 CSF3R 下游的 Janus 激酶 2 或 SRC 激酶信号是可行的，应该在治疗上进行探索。在此，我们讨论这些发现对这些疾病的分类和治疗的潜在影响。
