Transformation of mycosis fungoides: T-cell receptor beta gene analysis demonstrates a common clonal origin for plaque-type mycosis fungoides and CD30+ large-cell lymphoma.
Transformation of mycosis fungoides: T-cell receptor beta gene analysis demonstrates a common clonal origin for plaque-type mycosis fungoides and CD30+ large-cell lymphoma.
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蕈样肉芽肿的转化：T细胞受体β基因分析表明斑块型蕈样肉芽肿和CD30大细胞淋巴瘤有共同的克隆起源。
DOI：
10.1111/1523-1747.ep12365416
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发表时间：
1993
期刊：
影响因子：
--
通讯作者：
Levy,R
中科院分区：
文献类型：
--
作者：
Wood,GS;Bahler,DW;Hoppe,RT;Warnke,RA;Sklar,JL;Levy,R
众所周知，患有典型霉菌病(MF)的患者可能会发展成大细胞淋巴瘤(LCL)，这种现象被称为“转化”。关于MF转化的一个悬而未决的问题是，MF和LCL是代表两个不同的淋巴瘤，还是它们来自同一个T细胞克隆。我们报告了一例白人男性的MF和LCL的临床病理、免疫表型和免疫表型分析。他在51岁时出现了皮疹。在56岁时被诊断为临床期IA斑块/斑块MF。在局部氮芥末和全皮肤电子线治疗进行性全身性CD3+CD4+斑块/斑块病变后，他在72岁时出现了Ki-1+(CD30+)T-LCL结节。DNA经BG/II或BamHI消化后，用T细胞受体(TcR)-β基因Jβ1/Jβ2探针进行Southern杂交分析，在相隔4年获得的MF和LCL皮损中均有一条相同的单一重排条带。V-β基因家族特异性基因扩增结果显示，两种类型的皮损均以V-β-6PCR产物为主。这些聚合酶链式反应产物和皮损基因在TcR-β基因vdj联合引物扩增后，在能够分辨微小大小差异的条件下进行扩增，呈现出一种克隆的模式。此外，对从MF和LCL皮损中扩增的Vβ6PCR产物的序列分析显示，Vβ6.4、Dβ1.1、Jβ1.2和Cβ1的核苷酸序列完全相同。这些结果表明，该病例的MF和LCL都来自同一个T细胞克隆，这些疾病是在克隆的TCRTCR-β基因重排后的克隆分化阶段发展起来的。
It is well recognized that patients with classical mycosis fun-goides (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 clinico- pathologic, 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)-β gene Jβ1/Jβ2 probe showed a single, identical rearranged band in both the MF and LCL skin lesions that had been obtained 4 years apart. Vβ gene family – specific gene amplification assays demonstrated dominant Vβ6 PCR products in both types of lesions. These PCR products and lesional cDNA exhibited a monoclonal pattern when amplified with consensus TCR-β gene VDJ joint primers and electrophoresed under conditions that allowed the resolution of small differences in size. Furthermore, sequence analysis of the Vβ6 PCR products amplified from both the MF and LCL lesions showed an identical nucleotide sequence involving Vβ6.4, Dβ1.1, Jβ1.2, and Cβ1. 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-β gene.