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黏膜相关淋巴组织淋巴瘤的分子发病机制

Molecular Pathogenesis of MALT Lymphoma.

作者信息

Troppan Katharina, Wenzl Kerstin, Neumeister Peter, Deutsch Alexander

机构信息

Division of Hematology, Department of Internal Medicine, Medical University of Graz (MUG), 8036 Graz, Austria.

出版信息

Gastroenterol Res Pract. 2015;2015:102656. doi: 10.1155/2015/102656. Epub 2015 Apr 1.

DOI:10.1155/2015/102656
PMID:25922601
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4397421/
Abstract

Approximately 8% of all non-Hodgkin lymphomas are extranodal marginal zone B cell lymphoma of mucosa associated lymphoid tissue (MALT), also known as MALT lymphoma, which was first described in 1983 by Isaacson and Wright. MALT lymphomas arise at a wide range of different extranodal sites, with the highest frequency in the stomach, followed by lung, ocular adnexa, and thyroid, and with a low percentage in the small intestine. Interestingly, at least 3 different, apparently site-specific, chromosomal translocations and missense and frameshift mutations, all pathway-related genes affecting the NF-κB signal, have been implicated in the development and progression of MALT lymphoma. However, these genetic abnormalities alone are not sufficient for malignant transformation. There is now increasing evidence suggesting that the oncogenic product of translocation cooperates with immunological stimulation in oncogenesis, that is, the association with chronic bacterial infection or autoaggressive process. This review mainly discusses MALT lymphomas in terms of their genetic aberration and association with chronic infections and summarizes recent advances in their molecular pathogenesis.

摘要

所有非霍奇金淋巴瘤中约8%为黏膜相关淋巴组织边缘区B细胞淋巴瘤(MALT),也称为MALT淋巴瘤,它于1983年由艾萨克森和赖特首次描述。MALT淋巴瘤发生于多种不同的结外部位,其中胃的发生率最高,其次是肺、眼附属器和甲状腺,小肠中的发生率较低。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以及错义突变和移码突变,所有这些影响NF-κB信号的途径相关基因都与MALT淋巴瘤的发生和发展有关。然而,仅这些基因异常并不足以导致恶性转化。现在越来越多的证据表明,易位的致癌产物在肿瘤发生过程中与免疫刺激协同作用,即与慢性细菌感染或自身免疫过程相关。本综述主要从MALT淋巴瘤的基因畸变及其与慢性感染的关系方面进行讨论,并总结其分子发病机制的最新进展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e48/4397421/172fde0311ba/GRP2015-102656.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e48/4397421/172fde0311ba/GRP2015-102656.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e48/4397421/172fde0311ba/GRP2015-102656.001.jpg

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Nat Commun. 2015 Jan 8;6:5908. doi: 10.1038/ncomms6908.
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FOXP1 directly represses transcription of proapoptotic genes and cooperates with NF-κB to promote survival of human B cells.FOXP1直接抑制促凋亡基因的转录,并与NF-κB协同作用以促进人B细胞的存活。
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B-cell receptor signaling as a driver of lymphoma development and evolution.
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Infect Agent Cancer. 2024 Jul 27;19(1):33. doi: 10.1186/s13027-024-00597-0.
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Medicine (Baltimore). 2024 May 24;103(21):e38303. doi: 10.1097/MD.0000000000038303.
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