作者: P A Greif , M Yaghmaie , N P Konstandin , B Ksienzyk , K Alimoghaddam
DOI: 10.1038/LEU.2011.114
关键词:
摘要: The t(15;17) translocation that results in the PML/RARA fusion is disease-defining lesion nearly all cases of acute promyelocytic leukemia (APL).1 Despite importance for pathogenesis APL, it most likely not sufficient to cause leukemia. long latency, incomplete penetrance and additional cytogenetic changes accompanying onset progression disease murine APL models strongly suggest mutations are required development APL.2 In newly diagnosed patients with approximately 40% have leukemic cells secondary abnormalities.3 Collaborating affecting FLT3 receptor tyrosine kinase found about 20–30% a synergism between was also observed models.4