非特指型外周T细胞淋巴瘤FGR和TP73基因改变的研究

 目的　研究非特指型外周T细胞淋巴瘤（PTCL-NOS）中FGR和TP73的基因改变，验证前期基于芯片的比较基因组杂交（a-CGH）研究结果，为PTCL-NOS的发生、发展提供科学依据。方法　间期双色荧光原位杂交（FISH）技术检测34例PTCL-NOS（其中19例经过a-CGH检测）中FGR和TP73的基因改变，所用探针为缺口平移法自制的FGR和TP73特异位点探针以及商品化1号染色体着丝粒探针（CEP1）。结果　34例中出现基因改变者7例（20.6 %），其中FGR扩增1例，TP73扩增2例；FGR和TP73同时出现基因改变4 例（11.8 %），其中同时杂合性缺失（LOH）1例，同时扩增3例。CEP1扩增 4例（11.8 %），与TP73／FGR基因扩增同时存在。Kaplan-Meier生存分析显示基因改变组较基因无改变组以及TP73改变组较TP73无改变组均有预后不良的趋势，但差异无统计学意义（均P＞0.05）。结论　FISH结果部分验证了前期a-CGH的研究发现；淋巴瘤相关基因FGR和TP73改变以及1号染色体多倍体可能在PTCL-NOS的发生、发展中起着重要的作用。

Genetic aberration of FGR and TP73 in peripheral T cell lymphoma not otherwise specified

Objective To investigate the genetic changes of FGR and TP73 in PTCL-NOS, in order to verify the results of our previous a-CGH study and to explore their role on the pathogenesis of PTCL-NOS. Methods A total of 34 eases, of which 19 cases were examined by a-CGH, were investigated by interphasedual-colour FISH using homemade site-specific probes of FGR and TP73 by using a labelling method of nick translation and commercial probe CEP1. Results In general, 7 of 34 （20.6 %） cases of PTCL-NOS showed genetic aberrations, of which 4 cases had changes on both of the loci of FGR and TP73, including 3 cases of amplification and 1 loss of heterozygosity （LOH）, 1 case of FGR amplification and other 2 TP73 amplification only. CEP1 amplification was detected in 4 cases （11.8 %）, simuhaneously associated with FGR/ TP73 gene amplification. Kaplan-Meier survival analysis indicated there was a trend that the group with genetic changes had a poorer prognosis than the group of non-genetic changes, and so as the group of TP73 genetic changes compared with the group of TP73 non-genetic changes, although their was no statistical significance （P 〉0.05）. Conclusion The outcome of this study partially verified the resuhs of a-CGH, and aberration of lymphoma-related genes FGR and TP73, and the amplification of CEP1 may play a significant role in the pathogenesis of PTCL-NOS.