Journals / Experimed / 2022 / Cilt: 12 - Sayı: 3

Activation-Induced Cytidine Deaminase Expression in Patients with Chronic Myeloid Leukemia

Journal
Experimed
Pages
155–159
Publication Date
2022-12-31
DOI
—
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AI Summary & Key Takeaways

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

No significant relationship occurred in AID transcription levels with the tyrosine-kinase-inhibitor (TKI) resistant mutation profile or cytogenetic response during TKI therapy.Conclusion: This study found AID expression levels to be significantly elevated in CML patients and AID to be able to contribute to the etiopathogenesis of CML

📌 3 Key Takeaways

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Objective & Hypothesis:Objective: The findings on chronic myeloid leukemia (CML) patients suggest that clonal tumoral cells tend to have additional mutations besides the formation of the BCR-ABL fusion gene.
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Key Findings & Data:Previous studies have demonstrated abnormal activation-induced cytidine deaminase (AID) expression in various types of cancer, showing AID transcript levels to be elevated in the CML blast phase.
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Conclusion & Impact:No significant relationship occurred in AID transcription levels with the tyrosine-kinase-inhibitor (TKI) resistant mutation profile or cytogenetic response during TKI therapy.Conclusion: This study found AID expression levels to be significantly elevated in CML patients and AID to be able to contribute to the etiopathogenesis of CML
🔬Design:Research Article
📍Scope:Comprehensive Sample
⚙️Variables:Chronic myeloid leukemia · gene expression · cytidine deaminase

Abstract

Objective: The findings on chronic myeloid leukemia (CML) patients suggest that clonal tumoral cells tend to have additional mutations besides the formation of the BCR-ABL fusion gene. Previous studies have demonstrated abnormal activation-induced cytidine deaminase (AID) expression in various types of cancer, showing AID transcript levels to be elevated in the CML blast phase. The study aimed to investigate the AID gene expression levels in CML and to investigate the etiopathogenic role of AID, which is not yet fully understood.Materials and Methods: This study analyzed the AID transcript levels of 80 CML patients and 50 controls using real-time quantitative reverse transcription polymerase chain reaction (qRT-PCR).Results: The study found the AID transcript levels to be significantly elevated (p < 0.001) in the CML patients compared to the control group, with no significance in AID transcript levels with regard to the patients’ age, gender, clinical characteristics, or laboratory findings. No correlation was found between the AID and BCR-ABL transcript levels, while a positive correlation was present between AID transcript levels and presence of polymorphonuclear leukocytes (PMNL; r = 0.320, p = 0.021). No significant relationship occurred in AID transcription levels with the tyrosine-kinase-inhibitor (TKI) resistant mutation profile or cytogenetic response during TKI therapy.Conclusion: This study found AID expression levels to be significantly elevated in CML patients and AID to be able to contribute to the etiopathogenesis of CML

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Cite This Article

OGUZ, E., ADAY, A. D., YAVUZ, A. S. (2022). Activation-Induced Cytidine Deaminase Expression in Patients with Chronic Myeloid Leukemia. Experimed, Cilt: 12 - Sayı: 3, 155–159. https://ajindex.com/articles/878269

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References (14)

  1. Chereda B, Melo JV. Natural course and biology of CML. Ann Hematol 2015
  2. 94(Suppl 2): S107-21. [CrossRef] google scholar 2. Muramatsu M, Kinoshita K, Fagarasan S, Yamada S, Shinkai Y, Honjo T. Class switch recombination and hypermutation require activation-induced cytidine deaminase (AID), a potential RNA editing enzyme. Cell 2000
  3. 102(5): 553-63. [CrossRef] google scholar 3. Conticello SG. The AID/APOBEC family of nucleic acid mutators. Genome Biol 2008
  4. 9(6): 229. [CrossRef] google scholar 4. Sablitzky F, Wildner G, Rajewsky K. Somatic mutation and clonal expansion of B cells in an antigen-driven immune response. EMBO J 1985
  5. 4(2): 345-50. [CrossRef] google scholar 5. Rios LAS, Cloete B, Mowla S. Activation-induced cytidine deaminase: in sickness and in health. J Cancer Res Clin Oncol 2020
  6. 146(11): 2721-30. [CrossRef] google scholar 6. Hu D, Zheng H, Liu H, Li M, Ren W, Liao W, et al. Immunoglobulin expression and its biological significance in cancer cells. Cell Mol Immunol 2008
  7. 5(5): 319-24. [CrossRef] google scholar 7. Kunimoto H, McKenney AS, Meydan C, Shank K, Nazir A, Rapaport F, et al. Aid is a key regulator of myeloid/erythroid differentiation and DNA methylation in hematopoietic stem/progenitor cells. Blood 2017
  8. 129(13): 1779-90. [CrossRef] google scholar 8. Yu K, Huang FT, Lieber MR. DNA substrate length and surrounding sequence affect the activation-induced deaminase activity at cytidine. J Biol Chem 2004
  9. 279(8): 6496-500. [CrossRef] google scholar 9. Chen Z, Qiu X, Gu J. Immunoglobulin expression in non-lymphoid lineage and neoplastic cells. Am J Pathol 2009
  10. 174(4): 1139-48. [CrossRef] google scholar 10. Dominguez PM, Shaknovich R. Epigenetic function of activation-induced cytidine deaminase and its link to lymphomagenesis. Front Immunol 2014
  11. [CrossRef] google scholar 11. Feldhahn N, Henke N, Melchior K, Duy C, Soh BN, Klein F, et al. Activation-induced cytidine deaminase acts as a mutator in BCR-ABL1-transformed acute lymphoblastic leukemia cells. J Exp Med 2007
  12. 204(5): 1157-66. [CrossRef] google scholar 12. Maura F, Rustad EH, Yellapantula V,tuksza M, Hoyos D, Maclachlan KH, et al. Role of AID in the temporal pattern of acquisition of driver mutations in multiple myeloma. Leukemia 2020
  13. 34(5): 1476-80. [CrossRef] google scholar 13. Rebhandl S, Huemer M, Greil R, Geisberger R. AID/APOBEC deaminases and cancer. Oncoscience 2015
  14. 2(4): 320-33. [CrossRef] google scholar 14. Torun ES, Dağlar Aday A, Nalçaci M. Activation-induce