Donner L R, Dobin S, Harrington D, Bassion S, Rappaport E S, Peterson R F
Department of Pathology, Scott and White Memorial Hospital, Temple, TX 76508.
Cancer. 1990 Jan 15;65(2):249-54. doi: 10.1002/1097-0142(19900115)65:2<249::aid-cncr2820650212>3.0.co;2-y.
We report the occurrence of a cytogenetically abnormal clone 46,XX,t(1;6)(p35;q23),t(1;9;19)(q23;p24;q13) in the spleen of a 23-year-old woman with a three-year history of angiocentric immunoproliferative lesion (AIL) (lymphomatoid granulomatosis). The skin, lungs, spleen, liver and, focally, bone marrow were involved by atypical lymphohistiocytic infiltrates. Immunophenotypic study of the spleen showed that 46% of the cells displayed a helper/inducer T-cell phenotype. However, analysis of DNA isolated from the spleen failed to show clonal T-cell receptor beta-chain gene, T-cell receptor gamma-chain gene, or immunoglobulin heavy chain gene and light chain gene rearrangements. The finding of a cytogenetically abnormal clone supports the concept that angiocentric immunoproliferative lesion is a neoplastic process.
我们报告了一名23岁女性脾脏中出现细胞遗传学异常克隆46,XX,t(1;6)(p35;q23),t(1;9;19)(q23;p24;q13)的情况,该女性患有以血管为中心的免疫增殖性病变(AIL)(淋巴瘤样肉芽肿病)三年。皮肤、肺、脾、肝以及局部骨髓均有非典型淋巴组织细胞浸润。脾脏的免疫表型研究显示,46%的细胞表现为辅助/诱导性T细胞表型。然而,从脾脏分离的DNA分析未能显示克隆性T细胞受体β链基因、T细胞受体γ链基因或免疫球蛋白重链基因及轻链基因重排。细胞遗传学异常克隆的发现支持了以血管为中心的免疫增殖性病变是一种肿瘤性过程的概念。