Aberrant activation-induced cytidine deaminase expression in Philadelphia chromosome-positive B-cell acute lymphoblastic leukemia

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• 作者：Yang Shi ; MD ; PhD ^{yangshi11@gmail.com" class="auth_mail" title="E-mail the corresponding author} ; Xiaoxian Zhao ; PhD ^{Zhaox2@ccf.org" class="auth_mail" title="E-mail the corresponding author} ; Lisa Durkin ^{durkinl@ccf.org" class="auth_mail" title="E-mail the corresponding author} ; Heesun Joyce Rogers ; MD ; PhD ^{Rogersj5@ccf.org" class="auth_mail" title="E-mail the corresponding author} ; Eric D. Hsi ; MD ; ^{hsie@ccf.org" class="auth_mail" title="E-mail the corresponding author}
• 关键词：Activation-induced cytidine deaminase ; Acute lymphoblastic leukemia ; Philadelphia chromosome ; BCR-ABL1 ; Immunohistochemistry
• 刊名：Human Pathology
• 出版年：2016
• 出版时间：June 2016
• 年：2016
• 卷：52
• 期：Complete
• 页码：173-178
• 全文大小：710 K

文摘

Activation-induced cytidine deaminase (AID) is expressed in germinal center B cells and plays a critical role in somatic hypermutation and class-switch recombination of immunoglobulin genes. Philadelphia chromosome-positive (Ph+) acute lymphoblastic leukemia (ALL) carries a poor prognosis and is specifically treated with tyrosine kinase inhibitors. Interestingly, AID has been shown to be aberrantly expressed and functional in Ph+ ALL and is thought to contribute to genetic instability. We hypothesized that AID might be detectable in routinely processed bone marrow biopsies by immunohistochemistry (IHC) and assist in identifying Ph+ ALL. We found that AID was expressed in 26 (70%) of 37 cases of Ph+ ALL but only 1 (2.9%) of 38 cases of Ph− ALL cases. There was a significant difference in AID expression between these 2 ALL groups (P < .001, Fisher exact test). The expression of AID was confirmed by RT-PCR (reverse-transcriptase polymerase chain reaction) and correlated with IHC scoring. AID protein is expressed in a large proportion of Ph+ ALL cases at levels detectable by IHC in clinical samples and might be useful to rapidly identify cases likely to have a BCR/ABL1 fusion.