Davies Faith E, Dring Ann M, Li Cheng, Rawstron Andrew C, Shammas Masood A, O'Connor Sheila M, Fenton James A L, Hideshima Teru, Chauhan Dharminder, Tai Isabella T, Robinson Elizabeth, Auclair Daniel, Rees Karen, Gonzalez David, Ashcroft A John, Dasgupta Ranjit, Mitsiades Constantine, Mitsiades Nicholas, Chen Lan B, Wong Wing H, Munshi Nikhil C, Morgan Gareth J, Anderson Kenneth C
Academic Unit of Haematology and Oncology, Algernon Firth Bldg, School of Medicine, University of Leeds, Leeds, United Kingdom.
Blood. 2003 Dec 15;102(13):4504-11. doi: 10.1182/blood-2003-01-0016. Epub 2003 Aug 28.
To define specific pathways important in the multistep transformation process of normal plasma cells (PCs) to monoclonal gammopathy of uncertain significance (MGUS) and multiple myeloma (MM), we have applied microarray analysis to PCs from 5 healthy donors (N), 7 patients with MGUS, and 24 patients with newly diagnosed MM. Unsupervised hierarchical clustering using 125 genes with a large variation across all samples defined 2 groups: N and MGUS/MM. Supervised analysis identified 263 genes differentially expressed between N and MGUS and 380 genes differentially expressed between N and MM, 197 of which were also differentially regulated between N and MGUS. Only 74 genes were differentially expressed between MGUS and MM samples, indicating that the differences between MGUS and MM are smaller than those between N and MM or N and MGUS. Differentially expressed genes included oncogenes/tumor-suppressor genes (LAF4, RB1, and disabled homolog 2), cell-signaling genes (RAS family members, B-cell signaling and NF-kappaB genes), DNA-binding and transcription-factor genes (XBP1, zinc finger proteins, forkhead box, and ring finger proteins), and developmental genes (WNT and SHH pathways). Understanding the molecular pathogenesis of MM by gene expression profiling has demonstrated sequential genetic changes from N to malignant PCs and highlighted important pathways involved in the transformation of MGUS to MM.
为了确定在正常浆细胞(PCs)向意义未明的单克隆丙种球蛋白病(MGUS)和多发性骨髓瘤(MM)的多步骤转化过程中重要的特定途径,我们对来自5名健康供体(N)、7名MGUS患者和24名新诊断MM患者的PCs进行了微阵列分析。使用在所有样本中具有较大差异的125个基因进行无监督层次聚类,定义了2组:N组和MGUS/MM组。监督分析确定了在N组和MGUS组之间差异表达的263个基因,以及在N组和MM组之间差异表达的380个基因,其中197个基因在N组和MGUS组之间也存在差异调控。MGUS组和MM组样本之间仅74个基因差异表达,这表明MGUS组和MM组之间的差异小于N组和MM组或N组和MGUS组之间的差异。差异表达基因包括癌基因/肿瘤抑制基因(LAF4、RB1和失活同源物2)、细胞信号基因(RAS家族成员、B细胞信号和NF-κB基因)、DNA结合和转录因子基因(XBP1、锌指蛋白、叉头框和环指蛋白)以及发育基因(WNT和SHH途径)。通过基因表达谱分析了解MM的分子发病机制,已证明从N组到恶性PCs存在一系列基因变化,并突出了MGUS向MM转化过程中涉及的重要途径。