Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA; Department of Cell Biology, Harvard Medical School, Boston, MA, USA.
Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA.
Cancer Cell. 2019 Feb 11;35(2):283-296.e5. doi: 10.1016/j.ccell.2018.12.013. Epub 2019 Jan 31.
SF3B1 is recurrently mutated in chronic lymphocytic leukemia (CLL), but its role in the pathogenesis of CLL remains elusive. Here, we show that conditional expression of Sf3b1-K700E mutation in mouse B cells disrupts pre-mRNA splicing, alters cell development, and induces a state of cellular senescence. Combination with Atm deletion leads to the overcoming of cellular senescence and the development of CLL-like disease in elderly mice. These CLL-like cells show genome instability and dysregulation of multiple CLL-associated cellular processes, including deregulated B cell receptor signaling, which we also identified in human CLL cases. Notably, human CLLs harboring SF3B1 mutations exhibit altered response to BTK inhibition. Our murine model of CLL thus provides insights into human CLL disease mechanisms and treatment.
SF3B1 频繁发生突变的慢性淋巴细胞白血病 (CLL),但其在 CLL 的发病机制中的作用仍不清楚。在这里,我们表明 Sf3b1-K700E 突变条件表达在鼠 B 细胞中破坏前体 mRNA 剪接,改变细胞发育,并诱导细胞衰老状态。与 Atm 删除组合导致细胞衰老的克服和老年小鼠 CLL 样疾病的发展。这些 CLL 样细胞表现出基因组不稳定性和多个 CLL 相关细胞过程的失调,包括 B 细胞受体信号的失调,我们在人类 CLL 病例中也发现了这一点。值得注意的是,携带 SF3B1 突变的人类 CLL 对 BTK 抑制的反应发生改变。因此,我们的 CLL 小鼠模型为人类 CLL 疾病机制和治疗提供了新的见解。