髓系白血病
克隆(Java方法)
髓样
费城染色体
免疫学
医学
白血病
癌症研究
核型
祖细胞
生物
干细胞
造血
染色体
遗传学
基因
染色体易位
作者
Stefan Faderl,Moshe Talpaz,Zeev Estrov,Susan O’Brien,Razelle Kurzrock,Hagop M. Kantarjian
标识
DOI:10.1056/nejm199907153410306
摘要
Chronic myeloid leukemia (CML) is a clonal myeloproliferative expansion of transformed, primitive hematopoietic progenitor cells. It involves myeloid, monocytic, erythroid, megakaryocytic, B-lymphoid, and occasionally T-lymphoid lineages.1 CML was the first human disease in which a specific abnormality of the karyotype — the Philadelphia (Ph) chromosome — could be linked to pathogenetic events of leukemogenesis.2 It was among the first neoplastic diseases in which therapy with a biologic agent (interferon) was found to suppress the leukemic clone and prolong survival.3 Although heterogeneous, CML is the best-characterized leukemia at a molecular level, and studies in recent years have helped to define further . . .
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