Inaba Toshiya
Department of Molecular Oncology and Leukemia Program Project, Research Institute for Radiation Biology and Medicine, Hiroshima University.
Nihon Rinsho. 2009 Oct;67(10):1880-3.
Radiation induced acute myeloid leukemia (AML) was recognized a century ago, soon after mankind found radiation. Atomic bomb survivors developed de novo AML with relatively short latency with very high frequency. By contrast, excess occurrence of myelodysplastic syndrome (MDS) as well as solid tumors was found decades late. This difference may be due to etiology that many de novo AML patients harbor chimeric leukemogenic genes caused by chromosomal translocations, while MDS patients rarely carry chimeras. In addition, epigenetic change would play important roles. Therapy related leukemia is mainly caused by topoisomerase II inhibitors that cause de novo AML with an 11q23 translocation or by alkyrating agents that induce MDS/AML with an AML1 point mutation and monosomy 7.
辐射诱发的急性髓系白血病(AML)在一个世纪前人类发现辐射后不久就被认识到了。原子弹幸存者会以相对较短的潜伏期、非常高的频率患原发性AML。相比之下,骨髓增生异常综合征(MDS)以及实体瘤的过量发生是在几十年后才被发现的。这种差异可能归因于病因,许多原发性AML患者携带由染色体易位导致的嵌合致白血病基因,而MDS患者很少携带嵌合体。此外,表观遗传变化也起重要作用。治疗相关白血病主要由导致11q23易位的原发性AML的拓扑异构酶II抑制剂或导致具有AML1点突变和7号染色体单体的MDS/AML的烷化剂引起。