MALT lymphomas with API2(BIRC3)‐MALT1 translocation usually have an indolent clinical course and rarely transform into aggressive lymphoma, and there have been no lymphoma cell lines carrying API2‐MALT1 translocation reported to date. We established a novel lymphoma cell line named BMA19, carrying the API2‐MALT1 translocation from a patient with histologic transformation of intestinal MALT lymphoma. The cells were suggested to carry API2‐MALT1 and MYC‐IGH translocations by chromosomal analysis, and these translocations were confirmed by polymerase chain reaction analysis. The expression of MYC was shown to be enhanced as a result of the MYC‐IGH translocation, and it is considered to have played a role in the histologic transformation of MALT lymphoma. Whole exome sequencing of BMA19 identified several nucleotide variations in genes reported to be mutated in previous studies of marginal zone lymphomas. The MALT1 inhibitor MI‐2 specifically decreased cell growth, and the BMA19 cell line was suggested to be still dependent on the API2‐MALT1 signal. Subtractive microarray analysis showed that one of the earliest events resulting from MALT1 inhibition is increased susceptibility to endoplasmic reticulum stress‐induced apoptosis. The BMA19 cell line is considered to conserve the biological properties of MALT lymphoma and is expected to be a valuable tool for research into the pathogenesis of MALT lymphoma with an API2‐MALT1 translocation.

中文翻译：

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携带API2-MALT1易位的MALT淋巴瘤细胞系的建立和表征。

具有API2（BIRC3）-MALT1易位的MALT淋巴瘤通常临床病程缓慢，很少转化为侵袭性淋巴瘤，迄今为止，尚无携带API2-MALT1易位的淋巴瘤细胞系。我们建立了一种新型的淋巴瘤细胞系BMA19，该细胞系从患有肠道MALT淋巴瘤的组织学转变的患者中携带API2-MALT1易位。通过染色体分析，建议细胞携带API2-MALT1和MYC-IGH易位，并且通过聚合酶链反应分析确认这些易位。结果表明，MYC-IGH可增强MYC的表达易位，并被认为在MALT淋巴瘤的组织学转化中起作用。BMA19的整体外显子组测序鉴定了先前在边缘区淋巴瘤研究中据报道突变的基因中的几个核苷酸变异。MALT1抑制剂MI-2特异性地降低了细胞的生长，建议BMA19细胞株仍然依赖于API2-MALT1信号。减法微阵列分析表明，MALT1抑制引起的最早事件之一是对内质网应激诱导的细胞凋亡的敏感性增加。BMA19细胞系被认为可以保留MALT淋巴瘤的生物学特性，并有望成为研究API2-MALT1易位的MALT淋巴瘤发病机理的有价值的工具。