The pathogenesis of large cell transformation in cutaneous T-cell lymphoma is not associated with t(2;5)(p23;q35) chromosomal translocation.
The pathogenesis of large cell transformation in cutaneous T-cell lymphoma is not associated with t(2;5)(p23;q35) chromosomal translocation.
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皮肤T细胞淋巴瘤大细胞转化的发病机制与t(2;5)(p23;q35)染色体易位无关。
DOI：
10.1111/j.1600-0560.1997.tb00814.x
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发表时间：
1997
影响因子：
1.7
通讯作者：
Lessin,SR
中科院分区：
文献类型：
--
作者：
Li,G;Salhany,KE;Rook,AH;Lessin,SR
在20%-50%的晚期皮肤T细胞淋巴瘤（CTCL）中，恶性T细胞发生大细胞转化（LOT）。CTCL中LCT的恶性T细胞与CD 30（Ki-1）阳性间变性大细胞淋巴瘤（ALCL）在形态学和免疫表型上具有相似性，表明其发病机制相同。t（2; 5）（p23; q35）易位，导致核磷蛋白（NPM）基因和间变性淋巴瘤激酶（ALK）基因的融合，与原发性CD 30 + ALCL相关。为了确定这种染色体易位的获得是否参与CTCL中LCT的发病机制，我们检查了来自9名CTCL患者的12个肿瘤样本，包括8名LCT-CTCL患者和1名同时患有CTCL和霍奇金病的患者，t（2;5）易位的存在。4例LCT-CTCL中存在大量CD 30+大细胞，与继发性CD 30 + ALCL一致;另1例病例中CD 30在<10%的大细胞中表达，其他3例淋巴瘤中为阴性。使用跨越NPM/ALK融合连接的引物，mRNA逆转录（RT）后的PCR扩增未能显示所有检测样本中的NPM/ALK融合产物。因此，t（2;5）（p23;q35）易位似乎不参与CTCL（包括CD 30+病例）中LCT的分子发病机制。
In 20%–50% of the advanced cutaneous T‐cell lymphomas (CTCL), malignant T cells undergo large cell transformation (LOT). The malignant T cells of LCT in CTCL can share morphologic and immunophenotypic similarities with CD30 (Ki‐1)‐positive anaplastic large cell lymphoma (ALCL), suggesting a common mechanism of pathogenesis. The t(2;5) (p23;q35) translocation, resulting in the fusion of the nucleophosmin (NPM) gene and the anaplastic lymphoma kinase (ALK) gene, is associated with primary CD30+ ALCL.To determine whether acquisition of this chromosomal translocation is involved in the pathogenesis of LCT in CTCL, we examined 12 tumor samples from 9 CTCL patients, including 8 with LCT‐CTCL and one with concurrent CTCL and Hodgkin's disease, for the presence of the t(2;5) translocation. Numerous CD30+ large cells were present in 4 LCT‐CTCL consistent with secondary CD30+ ALCL; CD30 was expressed by <10% of the large cells in another case and was negative in the other 3 lymphomas. Using primers spanning the NPM/ALK fusion junction, PCR amplification following reverse transcription (RT) of mRNA failed to show the products of NPM/ALK fusion in all samples tested. Thus, the t(2;5) (p23;q35) translocation does not appear to be involved in the molecular pathogenesis of LCT in CTCL, including CD30+ cases.