Bertoni Francesco, Zucca Emanuele
Laboratory of Experimental Oncology and Lymphoma Unit, Oncology Institute of Southern Switzerland, Bellinzona, Switzerland.
J Clin Invest. 2006 Jan;116(1):22-6. doi: 10.1172/JCI27476.
Mucosa-associated lymphoid tissue (MALT) lymphomas can arise in a variety of extranodal sites. Interestingly, at least 3 different, apparently site-specific, chromosomal translocations, all affecting the NF-kappaB pathway, have been implicated in the development and progression of MALT lymphoma. The most common is the translocation t(11;18)(q21;q21), which results in a fusion of the cIAP2 region on chromosome 11q21 with the MALT1 gene on chromosome 18q21 and is present in more than one-third of cases. The frequency of this translocation is site-related: common in the gastrointestinal tract and lung, rare in conjunctiva and orbit, and almost absent in salivary glands, thyroid, liver, and skin. In this issue of the JCI, Hu et al. add to our understanding of the molecular consequences of this translocation, showing that its fusion product, cIAP2-MALT1, may concomitantly contribute to lymphomagenesis both as a tumor suppressor gene and as an oncogene.
黏膜相关淋巴组织(MALT)淋巴瘤可发生于多种结外部位。有趣的是,至少3种不同的、明显具有部位特异性的染色体易位,均影响核因子κB(NF-κB)信号通路,与MALT淋巴瘤的发生发展有关。最常见的是t(11;18)(q21;q21)易位,它导致11号染色体q21区域的cIAP2基因与18号染色体q21区域的MALT1基因融合,超过三分之一的病例存在该易位。这种易位的频率与部位相关:在胃肠道和肺部常见,在结膜和眼眶罕见,在唾液腺、甲状腺、肝脏和皮肤中几乎不存在。在本期《临床研究杂志》(JCI)中,Hu等人增进了我们对这种易位分子后果的理解,表明其融合产物cIAP2-MALT1可能作为肿瘤抑制基因和癌基因同时促进淋巴瘤的发生。