Xu Lian, Hunter Zachary R, Tsakmaklis Nicholas, Cao Yang, Yang Guang, Chen Jie, Liu Xia, Kanan Sandra, Castillo Jorge J, Tai Yu-Tzu, Zehnder James L, Brown Jennifer R, Carrasco Ruben D, Advani Ranjana, Sabile Jean M, Argyropoulos Kimon, Lia Palomba M, Morra Enrica, Trojani Alessandra, Greco Antonino, Tedeschi Alessandra, Varettoni Marzia, Arcaini Luca, Munshi Nikhil M, Anderson Kenneth C, Treon Steven P
Bing Center for Waldenström's Macroglobulinemia, Dana Farber Cancer Institute, Boston, MA, USA.
Department of Medicine, Harvard Medical School, Boston, MA, USA.
Br J Haematol. 2016 Mar;172(5):735-44. doi: 10.1111/bjh.13897. Epub 2015 Dec 13.
CXCR4(WHIM) somatic mutations are distinctive to Waldenström Macroglobulinaemia (WM), and impact disease presentation and treatment outcome. The clonal architecture of CXCR4(WHIM) mutations remains to be delineated. We developed highly sensitive allele-specific polymerase chain reaction (AS-PCR) assays for detecting the most common CXCR4(WHIM) mutations (CXCR4(S338X C>A and C>G) ) in WM. The AS-PCR assays detected CXCR4(S338X) mutations in WM and IgM monoclonal gammopathy of unknown significance (MGUS) patients not revealed by Sanger sequencing. By combined AS-PCR and Sanger sequencing, CXCR4(WHIM) mutations were identified in 44/102 (43%), 21/62 (34%), 2/12 (17%) and 1/20 (5%) untreated WM, previously treated WM, IgM MGUS and marginal zone lymphoma patients, respectively, but no chronic lymphocytic leukaemia, multiple myeloma, non-IgM MGUS patients or healthy donors. Cancer cell fraction analysis in WM and IgM MGUS patients showed CXCR4(S338X) mutations were primarily subclonal, with highly variable clonal distribution (median 35·1%, range 1·2-97·5%). Combined AS-PCR and Sanger sequencing revealed multiple CXCR4(WHIM) mutations in many individual WM patients, including homozygous and compound heterozygous mutations validated by deep RNA sequencing. The findings show that CXCR4(WHIM) mutations are more common in WM than previously revealed, and are primarily subclonal, supporting their acquisition after MYD88(L265P) in WM oncogenesis. The presence of multiple CXCR4(WHIM) mutations within individual WM patients may be indicative of targeted CXCR4 genomic instability.
CXCR4(WHIM)体细胞突变是华氏巨球蛋白血症(WM)所特有的,并且会影响疾病表现和治疗结果。CXCR4(WHIM)突变的克隆结构仍有待阐明。我们开发了高灵敏度的等位基因特异性聚合酶链反应(AS-PCR)检测方法,用于检测WM中最常见的CXCR4(WHIM)突变(CXCR4(S338X C>A和C>G))。AS-PCR检测方法在WM和意义未明的IgM单克隆丙种球蛋白病(MGUS)患者中检测到了Sanger测序未发现的CXCR4(S338X)突变。通过联合AS-PCR和Sanger测序,在未经治疗的WM、既往接受过治疗的WM、IgM MGUS和边缘区淋巴瘤患者中,分别有44/102(43%)、21/62(34%)、2/12(17%)和1/20(5%)检测到CXCR4(WHIM)突变,但慢性淋巴细胞白血病、多发性骨髓瘤患者、非IgM MGUS患者或健康供者中未检测到。对WM和IgM MGUS患者的癌细胞比例分析显示,CXCR4(S338X)突变主要为亚克隆性,克隆分布高度可变(中位数为35.1%,范围为1.2%-97.5%)。联合AS-PCR和Sanger测序在许多个体WM患者中发现了多个CXCR4(WHIM)突变,包括通过深度RNA测序验证的纯合和复合杂合突变。这些发现表明,CXCR4(WHIM)突变在WM中比之前所揭示的更为常见,并且主要是亚克隆性的,这支持了它们在WM肿瘤发生过程中在MYD88(L265P)之后获得这一观点。个体WM患者中存在多个CXCR4(WHIM)突变可能表明CXCR4基因组存在靶向性不稳定。