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弥漫性大 B 细胞淋巴瘤的分子发病机制。

Molecular pathogenesis of diffuse large B-cell lymphoma.

机构信息

Institute for Cancer Genetics and the Herbert Irving Comprehensive Cancer Center, and Department of Clinical Pathology and Cell Biology, Columbia University, New York, New York 10032, USA.

出版信息

Semin Diagn Pathol. 2011 May;28(2):167-77. doi: 10.1053/j.semdp.2011.04.001.

DOI:10.1053/j.semdp.2011.04.001
PMID:21842702
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3562715/
Abstract

In past years, substantial insight regarding the pathogenesis of diffuse large B-cell lymphoma has been obtained. Particularly, based on gene expression profile analysis, this disease can be classified into distinct phenotypic subgroups and specific transcriptional programs have been identified. New technologies like next-generation whole genome/exome sequencing and genome-wide single nucleotide polymorphism array analysis have revealed novel lesions involved in the pathogenesis of this disease. This review focuses on the diversity of genetic lesions identified in the different subtypes of diffuse large B-cell lymphoma.

摘要

在过去的几年中,人们对弥漫性大 B 细胞淋巴瘤的发病机制有了更深入的了解。特别是,基于基因表达谱分析,这种疾病可以分为不同的表型亚群,并且已经确定了特定的转录程序。下一代全基因组/外显子测序和全基因组单核苷酸多态性芯片分析等新技术揭示了涉及这种疾病发病机制的新病变。本综述重点介绍了弥漫性大 B 细胞淋巴瘤不同亚型中鉴定出的遗传病变的多样性。

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本文引用的文献

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Inactivating mutations of acetyltransferase genes in B-cell lymphoma.B 细胞淋巴瘤中乙酰转移酶基因的失活突变。
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The 2008 WHO classification of lymphoid neoplasms and beyond: evolving concepts and practical applications.2008 年世界卫生组织淋巴造血组织肿瘤分类及以后:不断发展的概念和实际应用。
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Somatic mutations at EZH2 Y641 act dominantly through a mechanism of selectively altered PRC2 catalytic activity, to increase H3K27 trimethylation.
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EZH2 Y641 上的体细胞突变通过选择性改变 PRC2 催化活性的机制发挥显性作用,从而增加 H3K27 三甲基化。
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