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首页> 外文期刊>The Journal of investigative dermatology. >Genomic alterations in blastic natural killer/extranodal natural killer-like T cell lymphoma with cutaneous involvement.
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Genomic alterations in blastic natural killer/extranodal natural killer-like T cell lymphoma with cutaneous involvement.

机译：皮肤受累的原始自然杀手/类体外自然杀手样T细胞淋巴瘤的基因组改变。

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Natural killer and natural killer-like T cell lymphomas represent a rare type of non-Hodgkin's lymphoma originally described to involve the upper aerodigestive tract. This malignancy has been increasingly observed in other extranodal sites, particularly in the skin. Patients with cutaneous natural killer cell lymphoma generally have a poor prognosis; however, the etiology and the underlying molecular pathogenesis remain unclear. This study aimed to investigate comprehensively genomic changes in blastic natural killer and extranodal natural killer-like T cell lymphoma with cutaneous involvement. Comparative genomic hybridization showed chromosome imbalances in six of eight cases studied (75%). The mean number of chromosome imbalances per sample was 2.18+/-1.63 with similar number of gains (1.18+/-1.17) and losses (1.00+/-1.34). The most frequent DNA copy number changes observed were losses of 9/9p (83%), followed by loss of 13q and gain of 7 (67%). Similar patterns of chromosome imbalances were observedin both blastic natural killer and cutaneous natural killer-like T cell lymphomas. Loss of the RB1 gene at 13q14.2 was detected in one blastic natural killer cell lymphoma with 13q loss using a gene dosage assay, and in one cutaneous natural killer-like T cell lymphoma without 13q loss using fluorescent in situ hybridization. Genomic microarray analysis identified oncogene copy number gains of PAK1 and JUNB in three of four cases studied, and gains of RAF1, CTSB, FGFR1, and BCR in two cases. Real-time polymerase chain reaction detected amplification of CTSB and RAF1 in four of five cases analyzed, JUNB and MYCN in three cases, and REL and YES1 in two cases, respectively. In conjunction with this study, an extensive literature search for the published G-banded karyotypes of four subsets of natural killer cell lymphomas was conducted, which showed a nonrandom pattern of multiple chromosome aberrations. These results reveal consistent genetic alterations in cutaneous natural killer cell lymphomas, and provide a basis for further investigation of molecular pathogenesis in this malignancy.
机译：天然杀伤性和类自然杀伤性T细胞淋巴瘤是一种罕见的非霍奇金淋巴瘤，最初被描述为累及上消化道。在其他结外部位，特别是在皮肤中，这种恶性现象越来越多地被观察到。皮肤自然杀伤细胞淋巴瘤患者一般预后较差;然而，病因和潜在的分子发病机制仍不清楚。这项研究旨在调查皮肤受累的原始自然杀手和结外自然杀手样T细胞淋巴瘤的基因组变化。比较的基因组杂交显示在研究的八例中有六例（75％）的染色体失衡。每个样本的染色体失衡的平均数为2.18 +/- 1.63，获得（1.18 +/- 1.17）和丢失（1.00 +/- 1.34）的次数相似。观察到的最频繁的DNA拷贝数变化是9 / 9p丢失（83％），其次是13q丢失和7增益（67％）。在原始自然杀手和皮肤自然杀手样T细胞淋巴瘤中均观察到相似的染色体失衡模式。使用基因剂量测定法，在一种13q丢失的原始自然杀伤细胞淋巴瘤中，使用基因剂量检测法在13q14.2处检测到RB1基因的丢失，而在荧光素原位杂交中，在一种13q丢失的皮肤自然杀伤性T细胞淋巴瘤中，检测到RB1基因的丢失。基因组微阵列分析确定了在研究的四例中的三例中，PAK1和JUNB的癌基因拷贝数增加，以及在二例中，RAF1，CTSB，FGFR1和BCR的增加。实时聚合酶链反应在5例中的4例中检测到CTSB和RAF1的扩增，JUNB和MYCN在3例中检测到，REL和YES1在2例中检测到。结合这项研究，进行了广泛的文献搜索，以查找四个自然杀伤细胞淋巴瘤亚组的已发表的G带核型，这显示了多个染色体畸变的非随机模式。这些结果揭示了皮肤自然杀伤细胞淋巴瘤中一致的遗传改变，并为进一步研究这种恶性分子发病机理提供了基础。

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