• Ege Sinan Torun, Aynur Dağlar Aday, and Meliha Nalçacı.
• Department of Internal Medicine, İstanbul Faculty of Medicine, İstanbul University, İstanbul, Turkey.
• Turk J Med Sci. 2021 Oct 21; 51 (5): 245124602451-2460.

Background/AimActivation-induced cytidine deaminase (AID) enables antibody diversity in B lymphocytes. It may also have an effect on MDS pathogenesis by causing somatic mutations and by inducing epigenetic changes in myeloid cells. This study aimed to compare AID expression of MDS patients with healthy controls, of MDS patients in different risk groups, and of MDS patients according to their treatment.Materials And MethodsTotal RNA was isolated and complementary DNA (cDNA) was transcribed from the peripheral blood samples of MDS patients and healthy controls. AID and the reference gene HPRT1 were analyzed using quantitative real-time PCR (QRT-PCR). AID expression relative to HPRT1 was calculated. Patients were classified into “lower risk” and “higher risk” subgroups according to their initial IPSS and IPSS-R scores and their MDS subtypes at the time of study. Patients were also divided into two groups based on receiving treatment with hypomethylating agents. AID expressions of different groups were compared using the Mann–Whitney U test.ResultsThirty MDS patients and thirty healthy controls were included. AID expression in MDS patients was significantly higher compared to healthy controls (p < 0.001). There was no significant difference in AID expression of “lower risk” and “higher risk” subgroups of patients. Patients that received hypomethylating agents did not have a significant difference in AID expression compared with patients that did not receive hypomethylating agents.ConclusionAID expression is increased in the peripheral blood of MDS patients compared to healthy controls. However, AID expression is not significantly different in “lower risk” and “higher risk” subgroups and in patients treated with hypomethylating agents. Increased AID expression may be an early step in MDS pathogenesis.This work is licensed under a Creative Commons Attribution 4.0 International License.

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