多发性骨髓瘤 (MM) 是一种临床疾病，其特征是骨髓微环境中浆细胞异常生长。在全球范围内，MM 的患病率一直在以惊人的速度稳步增长。在美国，2024年将诊断出超过30,000例癌症，约占癌症诊断的2%和癌症死亡的2%以上，是全球数字的两倍多。有症状和活动性 MM 的特点是浆细胞生长失控，导致严重肾功能损害、贫血、高钙血症和骨质流失。多种药物已获得 FDA 批准，现已广泛应用于 MM 的临床实践。尽管使用了三联体和四联体诱导方案、自体干细胞移植 (ASCT) 和维持治疗，但 MM 仍然是一种无法治愈的疾病，其特点是在其进展的各个阶段都可能发生复发。体弱、髓外疾病、浆细胞白血病、中枢神经系统复发、功能性高风险的多发性骨髓瘤患者以及老年人是目前未满足需求最多的人群。高昂的护理费用是另一个挑战。 MM细胞是高度蛋白质分泌细胞，因此依赖于某些翻译途径的激活。 MM 也很有可能改变核糖体蛋白编码基因，如 MYC 突变。在本文中，我们讨论了核糖体生物发生在促进 MM 和 RNA 聚合酶 I 抑制方面的重要性，作为即将到来的治疗方法，对 MM 患者具有潜在的前景。© 2024。作者。

Multiple myeloma (MM) is a clinical disorder characterized by aberrant plasma cell growth in the bone marrow microenvironment. Globally, the prevalence of MM has been steadily increasing at an alarming rate. In the United States, more than 30,000 cases will be diagnosed in 2024 and it accounts for about 2% of cancer diagnoses and more than 2% of cancer deaths, more than double the worldwide figure. Both symptomatic and active MM are distinguished by uncontrolled plasma cell growth, which results in severe renal impairment, anemia, hypercalcemia, and bone loss. Multiple drugs have been approved by the FDA and are now widely used in clinical practice for MM. Although triplet and quadruplet induction regimens, autologous stem cell transplantation (ASCT), and maintenance treatment are used, MM continues to be an incurable illness characterized by relapses that may occur at various phases of its progression. MM patients with frailty, extramedullary disease, plasma cell leukemia, central nervous system recurrence, functional high risk, and the elderly are among those with the greatest current unmet needs. The high cost of care is an additional challenge. MM cells are highly protein secretary cells and thus are dependent on the activation of certain translation pathways. MM also has a high chance of altering ribosomal protein-encoding genes like MYC mutation. In this article we discuss the importance of ribosome biogenesis in promoting MM and RNA polymerase I inhibition as an upcoming treatment with potential promise for MM patients.© 2024. The Author(s).