Stein Brady L, Oh Stephen T, Berenzon Dmitriy, Hobbs Gabriela S, Kremyanskaya Marina, Rampal Raajit K, Abboud Camille N, Adler Kenneth, Heaney Mark L, Jabbour Elias J, Komrokji Rami S, Moliterno Alison R, Ritchie Ellen K, Rice Lawrence, Mascarenhas John, Hoffman Ronald
Brady L. Stein, Northwestern Feinberg University School of Medicine, Chicago, IL; Stephen T. Oh and Camille Abboud, Washington University School of Medicine, St Louis, MO; Dmitriy Berenzon, Wake Forest University School of Medicine, Winston Salem, NC; Gabriela S. Hobbs, Massachusetts General Hospital, Boston, MA; Marina Kremyanskaya, John Mascarenhas, and Ronald Hoffman, Mount Sinai School of Medicine; Raajit K. Rampal, Memorial Sloan Kettering Cancer Center; Mark L. Heaney, Columbia University Medical Center; Ellen K. Ritchie, Cornell University School of Medicine, New York, NY; Kenneth Adler, Regional Cancer Care Associates, Morristown, NJ; Elias J. Jabbour, MD Anderson Cancer Center; Lawrence Rice, Cornell Houston Methodist Hospital, Houston, TX; Rami S. Komrokji, Moffitt Cancer Center, Tampa, FL; and Alison R. Moliterno, Johns Hopkins University School of Medicine, Baltimore, MD.
J Clin Oncol. 2015 Nov 20;33(33):3953-60. doi: 10.1200/JCO.2015.61.6474. Epub 2015 Aug 31.
Polycythemia vera (PV) is a chronic myeloproliferative neoplasm that is associated with a substantial symptom burden, thrombohemorrhagic complications, and impaired survival. A decade after the seminal discovery of an activating mutation in the tyrosine kinase JAK2 in nearly all patients with PV, new treatment options are finally beginning to emerge, necessitating a critical reappraisal of the underlying pathogenesis and therapeutic modalities available for PV. Herein, we comprehensively review clinical aspects of PV including diagnostic considerations, natural history, and risk factors for thrombosis. We summarize recent studies delineating the genetic basis of PV, including their implications for evolution to myelofibrosis and secondary acute myeloid leukemia. We assess the quality of evidence to support the use of currently available therapies, including aspirin, phlebotomy, hydroxyurea, and interferon. We analyze recent studies evaluating the safety and efficacy of JAK inhibitors, such as ruxolitinib, and evaluate their role in the context of other available therapies for PV. This review provides a framework for practicing hematologists and oncologists to make rational treatment decisions for patients with PV.
真性红细胞增多症(PV)是一种慢性骨髓增殖性肿瘤,伴有严重的症状负担、血栓出血并发症和生存受损。在几乎所有PV患者中发现酪氨酸激酶JAK2激活突变的开创性发现十年后,新的治疗选择终于开始出现,这就需要对PV的潜在发病机制和可用治疗方式进行批判性重新评估。在此,我们全面回顾PV的临床方面,包括诊断考量、自然病程以及血栓形成的危险因素。我们总结了最近描述PV遗传基础的研究,包括它们对向骨髓纤维化和继发性急性髓系白血病演变的影响。我们评估支持使用当前可用疗法(包括阿司匹林、放血、羟基脲和干扰素)的证据质量。我们分析最近评估JAK抑制剂(如鲁索替尼)安全性和有效性的研究,并评估它们在PV其他可用疗法背景下的作用。本综述为血液科医生和肿瘤内科医生为PV患者做出合理治疗决策提供了一个框架。