Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA.
Leukemia Service, Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA.
Sci Transl Med. 2014 May 28;6(238):238ra71. doi: 10.1126/scitranslmed.3008004.
Hairy cell leukemia (HCL) is a chronic lymphoproliferative disorder characterized by somatic BRAFV600E mutations. The malignant cell in HCL has immunophenotypic features of a mature B cell, but no normal counterpart along the continuum of developing B lymphocytes has been delineated as the cell of origin. We find that the BRAFV600E mutation is present in hematopoietic stem cells (HSCs) in HCL patients, and that these patients exhibit marked alterations in hematopoietic stem/progenitor cell (HSPC) frequencies. Quantitative sequencing analysis revealed a mean BRAFV600E-mutant allele frequency of 4.97% in HSCs from HCL patients. Moreover, transplantation of BRAFV600E-mutant HSCs from an HCL patient into immunodeficient mice resulted in stable engraftment of BRAFV600E-mutant human hematopoietic cells, revealing the functional self-renewal capacity of HCL HSCs. Consistent with the human genetic data, expression of BRafV600E in murine HSPCs resulted in a lethal hematopoietic disorder characterized by splenomegaly, anemia, thrombocytopenia, increased circulating soluble CD25, and increased clonogenic capacity of B lineage cells-all classic features of human HCL. In contrast, restricting expression of BRafV600E to the mature B cell compartment did not result in disease. Treatment of HCL patients with vemurafenib, an inhibitor of mutated BRAF, resulted in normalization of HSPC frequencies and increased myeloid and erythroid output from HSPCs. These findings link the pathogenesis of HCL to somatic mutations that arise in HSPCs and further suggest that chronic lymphoid malignancies may be initiated by aberrant HSCs.
毛细胞白血病(HCL)是一种慢性淋巴增生性疾病,其特征是体细胞 BRAFV600E 突变。HCL 中的恶性细胞具有成熟 B 细胞的免疫表型特征,但尚未确定沿发育中的 B 淋巴细胞连续体存在正常的对应细胞作为起源细胞。我们发现,HCL 患者的造血干细胞(HSCs)中存在 BRAFV600E 突变,并且这些患者表现出造血干细胞/祖细胞(HSPC)频率的明显改变。定量测序分析显示,HCL 患者的 HSCs 中 BRAFV600E 突变等位基因的平均频率为 4.97%。此外,将 HCL 患者的 BRAFV600E 突变 HSCs 移植到免疫缺陷小鼠中,导致 BRAFV600E 突变的人类造血细胞稳定植入,揭示了 HCL HSCs 的功能自我更新能力。与人类遗传数据一致,在小鼠 HSPCs 中表达 BRafV600E 导致一种致命的造血障碍,其特征是脾肿大、贫血、血小板减少、循环可溶性 CD25 增加以及 B 细胞谱系细胞的克隆形成能力增加——所有这些都是人类 HCL 的典型特征。相比之下,将 BRafV600E 的表达限制在成熟 B 细胞区室中不会导致疾病。用 vemurafenib(一种突变 BRAF 的抑制剂)治疗 HCL 患者,导致 HSPC 频率正常化,并增加 HSPC 产生的骨髓和红细胞输出。这些发现将 HCL 的发病机制与起源于 HSPCs 的体细胞突变联系起来,并进一步表明慢性淋巴细胞恶性肿瘤可能是由异常 HSCs 引发的。