Center of Research and Innovation of Myeloproliferative Neoplasms, Azienda Ospedaliera Universitaria Careggi and Department of Experimental and Clinical Medicine, University of Florence, Florence, Italy; and.
Department of Haematology, Guy's and St Thomas' National Health Service Foundation Trust, London, United Kingdom.
Blood. 2017 Feb 9;129(6):693-703. doi: 10.1182/blood-2016-10-695965. Epub 2016 Dec 27.
There has been a major revolution in the management of patients with myeloproliferative neoplasms (MPN), and in particular those with myelofibrosis and extensive splenomegaly and symptomatic burden, after the introduction of the JAK1 and JAK2 inhibitor ruxolitinib. The drug also has been approved as second-line therapy for polycythemia vera (PV). However, the therapeutic armamentarium for MPN is still largely inadequate for coping with patients' major unmet needs, which include normalization of life span (myelofibrosis and some patients with PV), reduction of cardiovascular complications (mainly PV and essential thrombocythemia), prevention of hematological progression, and improved quality of life (all MPN). In fact, none of the available drugs has shown clear evidence of disease-modifying activity, even if some patients treated with interferon and ruxolitinib showed reduction of mutated allele burden, and ruxolitinib might extend survival of patients with higher-risk myelofibrosis. Raised awareness of the molecular abnormalities and cellular pathways involved in the pathogenesis of MPN is facilitating the development of clinical trials with novel target drugs, either alone or in combination with ruxolitinib. Although for most of these molecules a convincing preclinical rationale was provided, the results of early phase 1 and 2 clinical trials have been quite disappointing to date, and toxicities sometimes have been limiting. In this review, we critically illustrate the current landscape of novel therapies that are under evaluation for patients with MPN on the basis of current guidelines, patient risk stratification criteria, and previous experience, looking ahead to the chance of a cure for these disorders.
在 JAK1 和 JAK2 抑制剂芦可替尼问世后,骨髓增殖性肿瘤(MPN)患者的治疗发生了重大变革,尤其是那些伴有骨髓纤维化、广泛脾肿大和症状负担的患者。该药还被批准用于治疗真性红细胞增多症(PV)的二线治疗。然而,MPN 的治疗手段仍然远远不能满足患者的主要未满足需求,这些需求包括延长寿命(骨髓纤维化和部分 PV 患者)、减少心血管并发症(主要是 PV 和原发性血小板增多症)、预防血液学进展以及提高生活质量(所有 MPN)。事实上,尚无任何可用药物显示出明确的疾病改善活性,即使一些接受干扰素和芦可替尼治疗的患者显示出突变等位基因负担减少,且芦可替尼可能延长高危骨髓纤维化患者的生存期。对 MPN 发病机制中涉及的分子异常和细胞途径的认识提高,促进了新型靶向药物的临床试验的发展,这些药物可单独使用或与芦可替尼联合使用。尽管对于大多数这些分子都提供了令人信服的临床前依据,但迄今为止早期 1 期和 2 期临床试验的结果相当令人失望,且毒性有时会限制其应用。在这篇综述中,我们根据现行指南、患者风险分层标准和以往经验,批判性地阐述了正在评估的用于 MPN 患者的新型治疗方法的现状,以期为这些疾病带来治愈的机会。