骨髓纤维化
红细胞生成
鲁索利替尼
骨髓增生性疾病
无效红细胞生成
医学
血液学
真性红细胞增多症
免疫学
癌症研究
骨髓
贫血
内科学
作者
William Vainchenker,Fabrizia Favale
出处
期刊:Leukemia
[Springer Nature]
日期:2013-06-01
卷期号:27 (6): 1219-1223
被引量:12
摘要
The term myeloproliferative disorders was introduced by William Dameshek1 in 1951 to describe four different diseases with a related pathogenesis: polycythaemia vera (PV), essential thrombocythaemia (ET), primary myelofibrosis (PMF) and chronic myeloid leukaemia. The discovery of the Philadelphia chromosome and the fusion gene BCR-ABL has permitted the definition of chronic myeloid leukaemia as a specific entity. The pathogenesis of the other non-BCR-ABL myeloproliferative disorders, now called myeloproliferative neoplasms (MPNs),2 remained elusive until 2005. At that time, these disorders were considered orphan disorders and were not the subject of intensive clinical interest. Nevertheless, it was clear that PV, ET and PMF had closely related pathogeneses, with some clinical, histological and biological features in common. This was underscored by the progression of some ETs to PVs, and some ETs or PVs to myelofibrosis, respectively called post-ET or post-PV myelofibrosis.
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