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目的研究弥漫大B细胞淋巴瘤(diffuse large B-cell lymphoma,DLBCL)的分子细胞遗传学异常,探讨DLBCL的分子细胞遗传学异常与临床特征的相关性。方法采用比较基因组杂交(comparative genomic hybridization,CGH)技术对24例DLBCL患者的全基因组遗传物质的扩增/缺失进行检测,分析CGH检测结果与DLBCL的临床特征及生存期的相关性。结果24例DLBCL中62·5%病例发生染色体水平的扩增/缺失,20·8%病例发生累及6q的缺失,16·7%病例发生累及18q扩增;CGH检测异常组与正常组比较CGH异常组患者Ann arbor分期多为Ⅱ~Ⅳ期,出现全身症状的几率较高,治疗疗效较差,生存期较短,但两组结果外累及发生几率无明显差别。结论基因组水平发生的遗传物质扩增/缺失是DLBCL常见的分子细胞遗传学异常;6q15-21缺失和18q11-ter扩增是DLBCL非随机分子细胞遗传学异常;CGH检测异常是DLBCL不良临床过程和预后标志。
Objective To investigate the molecular cytogenetic abnormalities of diffuse large B-cell lymphoma (DLBCL) and to explore the correlation between molecular cytogenetic abnormalities of DLBCL and clinical features. Methods The genomic DNA of 24 patients with DLBCL were detected by the method of comparative genomic hybridization (CGH), and the correlation between the CGH results and the clinical features and survival of DLBCL was analyzed. Results Chromosome amplification and deletion were found in 62.5% of DLBCL cases, 20.8% cases of 6q deletion cases and 16.7% cases of 18q cases. CGH was detected in abnormal group compared with normal group Ann arbor staging in patients with abnormal group mostly Ⅱ ~ Ⅳ stage, the higher the probability of systemic symptoms, poor efficacy of treatment, shorter survival, but the incidence of the two groups of patients with no significant difference in incidence and incidence. Conclusion Genome-wide amplification / deletion of genetic material is a common molecular cytogenetic abnormality in DLBCL. 6q15-21 deletion and 18q11-ter amplification are non-random molecular cytogenetic abnormalities in DLBCL. CGH abnormalities are the poor clinical course of DLBCL and Prognosis sign.