Greiner Timothy C, Dasgupta Chiranjib, Ho Vincent V, Weisenburger Dennis D, Smith Lynette M, Lynch James C, Vose Julie M, Fu Kai, Armitage James O, Braziel Rita M, Campo Elias, Delabie Jan, Gascoyne Randy D, Jaffe Elaine S, Muller-Hermelink Hans K, Ott German, Rosenwald Andreas, Staudt Louis M, Im Michael Y, Karaman Mazen W, Pike Brian L, Chan Wing C, Hacia Joseph G
Department of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, NE 68198, USA.
Proc Natl Acad Sci U S A. 2006 Feb 14;103(7):2352-7. doi: 10.1073/pnas.0510441103. Epub 2006 Feb 3.
Although mantle cell lymphoma (MCL) frequently harbors inactivated ataxia telangiectasia mutated (ATM) and p53 alleles, little is known about the molecular phenotypes caused by these genetic changes. We identified point mutations and genomic deletions in these genes in a series of cyclin D1-positive MCL cases and correlated genotype with gene expression profiles and overall survival. Mutated and/or deleted ATM and p53 alleles were found in 56% (40/72) and 26% (21/82) of the cases examined, respectively. Although MCL patients with inactive p53 alleles showed a significant reduction in median overall survival, aberrant ATM status did not predict for survival. Nevertheless, specific gene expression signatures indicative of the mutation and genomic deletion status of each gene were identified that were different from wild-type cases. These signatures were comprised of a select group of genes related to apoptosis, stress responses, and cell cycle regulation that are relevant to ATM or p53 function. Importantly, we found the molecular signatures are different between cases with mutations and deletions, because the latter are characterized by loss of genes colocalized in the same chromosome region of ATM or p53. This information on molecular phenotypes may provide new areas of investigation for ATM function or may be exploited by designing specific therapies for MCL cases with p53 aberrations.
尽管套细胞淋巴瘤(MCL)常存在共济失调毛细血管扩张突变(ATM)和p53等位基因失活的情况,但对于这些基因改变所导致的分子表型却知之甚少。我们在一系列细胞周期蛋白D1阳性的MCL病例中鉴定了这些基因的点突变和基因组缺失,并将基因型与基因表达谱及总生存率相关联。在所检测的病例中,分别有56%(40/72)和26%(21/82)的病例发现了ATM和p53等位基因的突变和/或缺失。尽管p53等位基因失活的MCL患者的中位总生存率显著降低,但异常的ATM状态并不能预测生存率。然而,我们鉴定出了指示每个基因的突变和基因组缺失状态的特定基因表达特征,这些特征与野生型病例不同。这些特征由一组与凋亡、应激反应和细胞周期调控相关的特定基因组成,这些基因与ATM或p53功能相关。重要的是,我们发现突变病例和缺失病例之间的分子特征不同,因为后者的特征是在ATM或p53的同一染色体区域共定位的基因缺失。这些关于分子表型的信息可能为ATM功能提供新的研究领域,或者可用于为p53异常的MCL病例设计特定疗法。