Wood G S, Bahler D W, Hoppe R T, Warnke R A, Sklar J L, Levy R
Department of Dermatology, Case Western Reserve University, Cleveland, Ohio.
J Invest Dermatol. 1993 Sep;101(3):296-300. doi: 10.1111/1523-1747.ep12365416.
It is well recognized that patients with classical mycosis fungoides (MF) may develop a large-cell lymphoma (LCL), a phenomenon known as "transformation." An unresolved issue regarding the transformation of MF is whether MF and LCL represent two separate lymphomas or whether they are derived from the same T-cell clone. We report the clinicopathologic, immunophenotypic, and immunogenotypic analysis of MF and LCL in a white male. He developed a rash at age 51 that was diagnosed at age 56 as clinical stage IA patch/plaque MF. After topical nitrogen mustard and total skin electron beam therapy for progressive generalized CD3+CD4+ patch/plaque lesions, he developed nodules of Ki-1+ (CD30+) T-LCL at age 72. Southern blot analysis of DNA digested with Bg/II or BamHI and probed with a T-cell receptor (TCR)-beta gene J beta 1/J beta 2 probe showed a single, identical rearranged band in both the MF and LCL skin lesions that had been obtained 4 years apart. V beta gene family--specific gene amplification assays demonstrated dominant V beta 6 PCR products in both types of lesions. These PCR products and lesional cDNA exhibited a monoclonal pattern when amplified with consensus TCR-beta gene VDJ joint primers and electrophoresed under conditions that allowed the resolution of small differences in size. Furthermore, sequence analysis of the V beta 6 PCR products amplified from both the MF and LCL lesions showed an identical nucleotide sequence involving V beta 6.4, D beta 1.1, J beta 1.2, and C beta 1. These findings indicate that both the MF and the LCL in this patient arose from the same T-cell clone and that these diseases developed at a stage in the clone's differentiation subsequent to rearrangement of the TCR-beta gene.
众所周知,经典蕈样肉芽肿(MF)患者可能会发展为大细胞淋巴瘤(LCL),这一现象被称为“转化”。关于MF转化的一个尚未解决的问题是,MF和LCL是代表两种不同的淋巴瘤,还是源自同一个T细胞克隆。我们报告了一名白人男性患者MF和LCL的临床病理、免疫表型和免疫基因分型分析。他51岁时出现皮疹,56岁时被诊断为临床IA期斑块/斑片型MF。在接受局部氮芥和全身皮肤电子束治疗以治疗进行性全身性CD3 + CD4 +斑块/斑片病变后,他72岁时出现了Ki-1 +(CD30 +)T-LCL结节。用Bg/II或BamHI消化并用T细胞受体(TCR)-β基因Jβ1/Jβ2探针杂交的DNA进行Southern印迹分析显示,在相隔4年获得的MF和LCL皮肤病变中均出现了单一、相同且重排的条带。Vβ基因家族特异性基因扩增检测显示,两种病变中均以Vβ6 PCR产物为主。当用共有TCR-β基因VDJ连接引物扩增并在能够分辨大小微小差异的条件下进行电泳时,这些PCR产物和病变cDNA呈现出单克隆模式。此外,对从MF和LCL病变中扩增的Vβ6 PCR产物进行序列分析显示,涉及Vβ6.4、Dβ1.1、Jβ1.2和Cβ1的核苷酸序列相同。这些发现表明,该患者的MF和LCL均源自同一个T细胞克隆,并且这些疾病是在TCR-β基因重排后克隆分化的一个阶段发生的。