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Waldenstr?m macroglobulinemia: biology genetics and therapy

機(jī)譯：Waldenstr?m巨球蛋白血癥：生物學(xué)遺傳學(xué)和治療

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Waldenström macroglobulinemia (WM) is a distinct clinicopathologic entity characterized by the presence of a lymphoplasmacytic lymphoma, a non-Hodgkin lymphoma, and IgM monoclonal gammopathy. WM is an indolent, uncommon malignancy mostly affecting the elderly. Patient outcomes have modestly improved since the introduction of rituximab to conventional cytotoxic chemotherapy more than 20 years ago. However, the pivotal discovery of the somatic MYD88 L265P mutation, harbored by most patients with WM, and the somatic CXCR4 WHIM mutations, similar to germline CXCR4 mutations seen in the warts, hypogammaglobulinemia, immunodeficiency, and myelokathexis (WHIM) syndrome, present in approximately one-third of patients with WM, has fundamentally changed our understanding of this disease and expanded the potential therapeutic targets. Within this new paradigm, ibrutinib emerged as a promising new drug. Ibrutinib targets Bruton’s tyrosine kinase, a downstream protein in the B-cell receptor pathway that is overactivated by the MYD88 L265P mutation. A seminal Phase II trial of ibrutinib in previously treated WM patients showed impressive response rates and confirmed the effects of MYD88 L265P and CXCR4 WHIM mutations in response to therapy. Ibrutinib is the first and only US Food and Drug Administration–approved drug specifically for the treatment of WM. However, before ibrutinib can be established as the standard of care for WM, long-term data regarding efficacy and safety are required. Further research to address ibrutinib resistance and cost-effectiveness is also imperative before ibrutinib can gain widespread acceptance. This review will cover the present pathophysiologic understanding of WM in light of the recent MYD88 and CXCR4 discovery, as well as current and emergent treatment regimens with focus on ibrutinib.
機(jī)譯：Waldenstr?m巨球蛋白血癥（WM）是一種獨(dú)特的臨床病理學(xué)實體，其特征是存在淋巴漿細(xì)胞性淋巴瘤，非霍奇金淋巴瘤和IgM單克隆丙種球蛋白病。 WM是一種惰性的，罕見的惡性腫瘤，主要影響老年人。自20多年前將利妥昔單抗引入常規(guī)細(xì)胞毒性化療以來，患者的治療效果已有所改善。但是，大多數(shù)WM患者都存在的體細(xì)胞MYD88 L265P突變和體細(xì)胞CXCR4 WHIM突變的關(guān)鍵發(fā)現(xiàn)，類似于在疣，低血球蛋白血癥，免疫缺陷和骨髓?。╓HIM）綜合征中發(fā)現(xiàn)的種系CXCR4突變。三分之一的WM患者從根本上改變了我們對這種疾病的認(rèn)識，并擴(kuò)大了潛在的治療目標(biāo)。在這種新的范例中，依魯替尼出現(xiàn)了一種有希望的新藥。依魯替尼靶向布魯頓酪氨酸激酶，后者是B細(xì)胞受體途徑中的下游蛋白，被MYD88 L265P突變過度激活。依魯替尼在先前接受過治療的WM患者中進(jìn)行的開創(chuàng)性II期臨床試驗顯示出令人印象深刻的緩解率，并證實了MYD88 L265P和CXCR4 WHIM突變對治療的響應(yīng)。依魯替尼是美國食品藥品監(jiān)督管理局批準(zhǔn)的首個也是唯一一個專門用于治療WM的藥物。但是，在將依魯替尼確立為WM的治療標(biāo)準(zhǔn)之前，需要有關(guān)療效和安全性的長期數(shù)據(jù)。在依魯替尼獲得廣泛認(rèn)可之前，還需要進(jìn)一步研究以解決依魯替尼的耐藥性和成本效益問題。鑒于最近的MYD88和CXCR4發(fā)現(xiàn)，以及針對依魯替尼的當(dāng)前和緊急治療方案，本綜述將涵蓋WM的當(dāng)前病理生理學(xué)理解。

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