Activation Induced Cytidine Deaminase Expression in Patients with Myelodysplastic Syndrome and its Relationship with Prognosis and Treatment.


Creative Commons License

Torun E. S. , Aday A. , Nalçaci M.

Turkish journal of medical sciences, vol.51, pp.2451-2460, 2021 (Peer-Reviewed Journal) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 51
  • Publication Date: 2021
  • Doi Number: 10.3906/sag-2101-81
  • Journal Name: Turkish journal of medical sciences
  • Journal Indexes: Science Citation Index Expanded, Scopus, Academic Search Premier, CAB Abstracts, EMBASE, MEDLINE, Veterinary Science Database, TR DİZİN (ULAKBİM)
  • Page Numbers: pp.2451-2460
  • Keywords: Activation induced cytidine deaminase, hypomethylating agents, myelodysplastic syndrome, CLASS-SWITCH RECOMBINATION, DNMT3A MUTATIONS, AID EXPRESSION, SCORING SYSTEM, DNA, TET2, 5-METHYLCYTOSINE, METHYLATION, MODULATION, MUTATOR

Abstract

Background/aim: Activation-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 methods: Total 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. Results: Thirty 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. Conclusion: AID 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.