Plasmablastic lymphoma with MYC translocation: evidence for a common pathway in the generation of plasmablastic features.
Plasmablastic lymphoma with MYC translocation: evidence for a common pathway in the generation of plasmablastic features.
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DOI：
10.1038/modpathol.2010.72
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发表时间：
2010-07
期刊：
影响因子：
--
通讯作者：
Jaffe ES
中科院分区：
文献类型：
--
作者：
Taddesse-Heath L;Meloni-Ehrig A;Scheerle J;Kelly JC;Jaffe ES
浆母细胞淋巴瘤被认为是弥漫性大b细胞淋巴瘤的一种亚型，它与浆细胞骨髓瘤的浆母细胞转化具有许多相似的形态学和免疫表型特征。在人类免疫缺陷病毒（HIV）感染的情况下，两种类型的肿瘤都可能与eb病毒（EBV）相关，因此使它们的区分具有挑战性。此外，这些实体之间的生物学关系尚不清楚。我们报告四个独特的病例浆母细胞淋巴瘤发生在设置艾滋病毒感染，有重叠的临床和遗传特征浆细胞骨髓瘤。我们回顾了临床、形态学和细胞遗传学的发现，并使用MYC分离重排探针进行了免疫组织化学、EBV原位杂交、染色体分析和荧光原位杂交（FISH）。所有患者均为男性，中位年龄45岁。除了结外病变、浆母细胞性淋巴瘤的形态和表型特征外，4例中有3例的临床表现也与浆细胞性骨髓瘤重叠，即单克隆血清免疫球蛋白和溶解性骨病变。此外，这些病例表现出在浆细胞骨髓瘤中更常见的复杂的细胞遗传学变化。一个独特的特征是存在MYC （8q24.1）重排，这在所有4例中都被FISH证实。MYC易位与多发性骨髓瘤的肿瘤进展有关，但在浆母细胞淋巴瘤中很少有报道。这些病例显示浆母细胞淋巴瘤与浆细胞骨髓瘤浆母细胞变体之间的临床和生物学关系。MYC的失调可能是一种共同的遗传机制，赋予b细胞肿瘤在分化后期的浆母细胞形态和侵袭性临床过程。
Plasmablastic lymphoma, which is considered a subtype of diffuse large B-cell lymphoma, shares many similar morphological and immunophenotypic features with plasmablastic transformation of plasma cell myeloma. In the setting of human immunodeficiency virus (HIV) infection, both types of neoplasms can be associated with Epstein–Barr virus (EBV), thus making their distinction challenging. Moreover, the biological relationship between these entities remains unclear. We report four unique cases of plasmablastic lymphoma occurring in the setting of HIV infection that had overlapping clinical and genetic features with plasma cell myeloma. We reviewed the clinical, morphological, and cytogenetic findings and performed immunohistochemistry, in situ hybridization for EBV, chromosome analysis, and fluorescent in situ hybridization (FISH) using the MYC break-apart rearrangement probe. All patients were males with a median age of 45 years. In addition to extra-nodal disease, plasmablastic morphology, and phenotype typical of plasmablastic lymphoma, three of the four cases also showed clinical findings overlapping with plasma cell myeloma, that is, monoclonal serum immunoglo-bulin and lytic bone lesions. Furthermore, these cases showed complex cytogenetic changes that are more commonly observed in plasma cell myeloma. A unique feature was the presence of MYC (8q24.1) rearrangement confirmed by FISH in all four cases. MYC translocation has been associated with tumor progression in multiple myeloma but has only rarely been previously reported in plasmablastic lymphoma. These cases show a clinical and biological relationship between plasmablastic lymphoma and the plasmablastic variant of plasma cell myeloma. Dysregulation of MYC may be a common genetic mechanism that imparts plasmablastic morphology and aggressive clinical course to B-cell neoplasms at a later stage of differentiation.
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