胞苷脱氨酶
活化诱导(胞苷)脱氨酶
体细胞突变
慢性淋巴细胞白血病
染色体易位
生物
癌症研究
胞嘧啶
白血病
骨髓
体细胞
基因
分子生物学
B细胞
遗传学
免疫学
抗体
作者
Metin Yusuf Gelmez,Başak Akadam-Teker,Aynur Dağlar Aday,Akif Selim Yavuz,Teoman Soysal,Günnur Deniz,Melih Aktan
标识
DOI:10.3109/10428194.2013.803225
摘要
Activation induced cytidine deaminase (AID) enzyme, which converts cytosine into uracil and is expressed only by activated B lymphocytes, plays a role in B cells in both the mechanisms of somatic hypermutation (SHM) and class switch recombination (CSR). There are studies showing that AID can cause numerous translocations in different lymphoproliferative diseases. Chronic lymphocytic leukemia (CLL) is characterized by the accumulation of monoclonal B cells in bone marrow and peripheral blood. The predictability and clinical status of B-CLL are difficult to determine. About 30–50% of patients have chromosomal abnormalities. AID, which is thought to create fraction segments for translocations, might also cause deletions in DNA regions of 17p13, 11q22.3, 13q14 and 13q34 that are associated with prognostic implications in patients with CLL. In this study, the AID gene expression in patients with CLL with and without deletions was investigated. When compared to healthy subjects and patients without deletions, increased levels of AID expression in patients with deletions of 17p13, 11q22.3 or 13q14 were found, but not for the 13q34 region. Our results show that AID expression may be associated with deletions in patients with CLL.
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