Van Etten Richard A
Molecular Oncology Research Institute and the Division of Hematology/Oncology, Tufts-New England Medical Center, Boston, MA 02111, USA.
J Exp Med. 2007 Mar 19;204(3):461-5. doi: 10.1084/jem.20062335. Epub 2007 Mar 12.
Chronic myeloid leukemia (CML), which is caused by the BCR-ABL fusion tyrosine kinase, is one of the most intensively studied human cancers. ABL kinase inhibitors have been spectacularly successful in treating CML, but disease persistence and acquired drug resistance can prevent eradication and cure of the leukemia. The development of better therapies will depend on a full understanding of signaling pathways in CML, facilitated by model studies using mutant mice.
慢性粒细胞白血病（CML）由BCR-ABL融合酪氨酸激酶引起，是研究最为深入的人类癌症之一。ABL激酶抑制剂在治疗CML方面取得了显著成功，但疾病的持续存在和获得性耐药可能会阻碍白血病的根除和治愈。更好疗法的开发将依赖于对CML信号通路的全面理解，而使用突变小鼠的模型研究将有助于实现这一点。
