Acquisition of Genetic Aberrations by Activation-Induced Cytidine Deaminase (AID) during Inflammation-Associated Carcinogenesis.
Acquisition of Genetic Aberrations by Activation-Induced Cytidine Deaminase (AID) during Inflammation-Associated Carcinogenesis.
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DOI：
10.3390/cancers3022750
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发表时间：
2011-06-22
期刊：
影响因子：
5.2
通讯作者：
Chiba T
中科院分区：
文献类型：
--
作者：
Takai A;Marusawa H;Chiba T
在各种肿瘤相关基因中积累的核苷酸改变和染色体异常等遗传异常在癌症的发展中起着重要作用。然而，获得遗传异常的确切机制仍不清楚。激活诱导型胞苷脱氨酶(AID)是一种核苷酸编辑酶，对抗体产生的多样化至关重要。AID仅在生理条件下激活的B淋巴细胞中表达，并在免疫球蛋白基因中诱导体细胞超突变和类开关重组。炎症导致多种胃肠道器官中AID的异常表达，AID表达的增加通过诱导上皮细胞的遗传改变而促进癌症的发生。对AID如何导致遗传疾病的研究有望阐明炎症相关致癌的机制。
Genetic abnormalities such as nucleotide alterations and chromosomal disorders that accumulate in various tumor-related genes have an important role in cancer development. The precise mechanism of the acquisition of genetic aberrations, however, remains unclear. Activation-induced cytidine deaminase (AID), a nucleotide editing enzyme, is essential for the diversification of antibody production. AID is expressed only in activated B lymphocytes under physiologic conditions and induces somatic hypermutation and class switch recombination in immunoglobulin genes. Inflammation leads to aberrant AID expression in various gastrointestinal organs and increased AID expression contributes to cancer development by inducing genetic alterations in epithelial cells. Studies of how AID induces genetic disorders are expected to elucidate the mechanism of inflammation-associated carcinogenesis.