Journals / Turkish Journal of Medical Sciences / 2021 / Cilt: 51 - Sayı: 5

Activation-induced cytidine deaminase expression in patients with myelodysplastic syndrome and its relationship with prognosis and treatment

Pages
2451–2460
Publication Date
2022-11-06
DOI
—
🏛️Bibliographic metadata and full text access for this article are provided via DergiPark.
DergiPark Record ↗
✨

AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

Increased AID expression may be an early step in MDS pathogenesis.Key words: Activation induced cytidine deaminase, hypomethylating agents, myelodysplastic syndrome

📌 3 Key Takeaways

🎯
Objective & Hypothesis:Background/aim: Activation-induced cytidine deaminase (AID) enables antibody diversity in B lymphocytes.
📊
Key Findings & Data:AID and the reference gene HPRT1 were analyzed using quantitative real-time PCR (QRT-PCR).
💡
Conclusion & Impact:Increased AID expression may be an early step in MDS pathogenesis.Key words: Activation induced cytidine deaminase, hypomethylating agents, myelodysplastic syndrome
🔬Design:Research Article
📍Scope:Comprehensive Sample
⚙️Variables:Domain Parameters

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.Key words: Activation induced cytidine deaminase, hypomethylating agents, myelodysplastic syndrome

🔖

Cite This Article

ADAY, A. D., NALÇACI, M., TORUN, E. S. (2022). Activation-induced cytidine deaminase expression in patients with myelodysplastic syndrome and its relationship with prognosis and treatment. Turkish Journal of Medical Sciences, Cilt: 51 - Sayı: 5, 2451–2460. https://ajindex.com/articles/609375

📄 Full Text PDF Viewer

📄

PDF görüntüleyici hazırlanıyor...

References (2)

  1. Wang ES, Berliner N. Hematopoiesis and hematopoietic failure. In: Andreoli TE, Benjamin IJ, Griggs RC, Wing EJ (editors). Andreoli and Carpenter's Cecil Essentials of Medicine. 8th ed. Philadelphia, PA, USA: Saunders/Elsevier; 2010. pp. 503-506
  2. Garcia-Manero G. Myelodysplastic syndromes: 2015 Update on diagnosis, risk-stratification and management. American Journal of Hematology 2015; 90: 831-841. doi: 10.1002/ajh.24102 3. Itzykson R, Fenaux P. Epigenetics of myelodysplastic syndromes. Leukemia 2014; 28: 497-506. doi: 10.1038/leu.2013.343 4. Visconte V, Tiu RV, Rogers HJ. Pathogenesis of myelodysplastic syndromes: an overview of molecular and non-molecular aspects of the disease. Blood research 2014; 49 (4): 216-227. doi: 10.5045/br.2014.49.4.216 5. Thol F, Winschel C, Lüdeking A, Yun H, Friesen I et al. Rare occurrence of DNMT3A mutations in myelodysplastic syndromes. Haematologica 2011; 96: 1870-1873. doi: 10.3324/haematol.2011.045559 6. Challen GA, Sun D, Jeong M, Luo M, Jelinek J et al. Dnmt3a is essential for hematopoietic stem cell differentiation. Nature Genetics 2011; 44: 23-31. doi: 10.1038/ng.1009 7. Walter MJ, Ding L, Shen D, Shao J, Grilot M et al. Recurrent DNMT3A mutations in patients with myelodysplastic syndromes. Leukemia 2011; 25: 1153-1158. doi: 10.1038/leu.2011.44 8. Ko M, An J, Bandukwala HS, Chavez L, Aijö T et al. Modulation of TET2 expression and 5-methylcytosine oxidation by the CXXC domain protein IDAX. Nature 2013; 497: 122-126. doi: 10.1038/nature12052 9. Ponnaluri VK, Maciejewski JP, Mukherji M. A mechanistic overview of TET-mediated 5-methylcytosine oxidation. Biochemical and Biophysical Research Communications 2013; 436: 115-120. doi: 10.1016/j.bbrc.2013.05.077 10. Jankowska AM, Szpurka H, Tiu RV, Makishima H, Afable M et al. Loss of heterozygosity 4q24 and TET2 mutations associated with myelodysplastic/myeloproliferative neoplasms. Blood 2009; 113: 6403-6410. doi: 10.1182/blood-2009-02-205690 11. Langemeijer SM, Kuiper RP, Berends M, Knops R, Aslanyan MG et al. Acquired mutations in TET2 are common in myelodysplastic syndromes. Nature Genetics 2009; 41: 838- 842. doi: 10.1038/ng.391 12. Smith AE, Mohamedali AM, Kulasekararaj A, Lim Z, Gäken J et al. Next-generation sequencing of the TET2 gene in 355 MDS and CMML patients reveals low-abundance mutant clones with early origins, but indicates no definite prognostic value. Blood 2010; 116: 3923-3932. doi: 10.1182/blood-2010- 03-274704 13. Kihara R, Nagata Y, Kiyoi H, Kato