title: Investigation of AID, Dicer, and Drosha Expressions in Patients with Chronic Lymphocytic Leukemia.
abstract: Chronic lymphocytic leukemia (CLL) is the most common leukemia in Western countries. Cytogenetic lesions such as del13q14, del11q22.3, and del17p13 are identified in 50-60% of patients. Activation-induced cytidine deaminase (AID) plays a central role in somatic hyper mutation (SHM) and class switch recombination (CSR) and functions on Ig genes, but also target non-Ig genes, and over-expression of AID can lead to point mutations or translocations in non-Ig genes such as IgH/Myc translocation. Dicer and Drosha, which have a role in activation process of miRNA, also act in a double-strand DNA break (DSB) repair mechanism. In this study, whether the changes of AID, Dicer and Drosha expressions may be associated with both deletions and clinical outcomes in patients with CLL were investigated. AID expressions were increased in patients with CLL. However, cell lysate AID protein levels were only increased in patients with del17p or del11q who have poor prognosis. Decreased Dicer expressions were found in patients with deletion, whereas increased Drosha expressions were found in patients without deletion and with del13q. According to Rai and Binet staging systems, advanced-stage patients showed increased AID protein levels, decreased Dicer and Drosha expressions. Our findings may suggest that high AID expression and lower Dicer expression were observed in patients with CLL especially del17p and del11q and might associated with deletions such as del17p and del11q. AID, Dicer, and Drosha expressions might be used as an indicator of prognosis for CLL.
authors.affiliation: a Department of Immunology, Institute of Experimental Medicine (DETAE) , Istanbul University , Istanbul , Turkey.
authors.forename: Metin Yusuf
authors.initials: MY
authors.lastname: Gelmez
authors.affiliation: b Division of Medical Genetic, Istanbul Faculty of Medicine , Istanbul University , Istanbul , Turkey.
authors.forename: Ender
authors.initials: E
authors.lastname: Coskunpinar
authors.affiliation: c Division of Hematology, Istanbul Faculty of Medicine , Istanbul University , Istanbul , Turkey.
authors.forename: Basak
authors.initials: B
authors.lastname: Saracoglu
authors.affiliation: a Department of Immunology, Institute of Experimental Medicine (DETAE) , Istanbul University , Istanbul , Turkey.
authors.forename: Gunnur
authors.initials: G
authors.lastname: Deniz
authors.affiliation: c Division of Hematology, Istanbul Faculty of Medicine , Istanbul University , Istanbul , Turkey.
authors.forename: Melih
authors.initials: M
authors.lastname: Aktan
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D016022:Case-Control Studies; D002872:Chromosome Deletion; D002880:Chromosomes, Human, Pair 11; D002882:Chromosomes, Human, Pair 13; D002886:Chromosomes, Human, Pair 17; D003564:Cytidine Deaminase / Q000235:genetics* / Q000378:metabolism; D053487:DEAD-box RNA Helicases / Q000235:genetics* / Q000378:metabolism; D005260:Female; D015973:Gene Expression Regulation, Leukemic; D006801:Humans; D015451:Leukemia, Lymphocytic, Chronic, B-Cell / Q000175:diagnosis* / Q000235:genetics / Q000473:pathology; D007963:Leukocytes, Mononuclear / Q000378:metabolism / Q000473:pathology; D008297:Male; D035683:MicroRNAs / Q000235:genetics / Q000378:metabolism; D008875:Middle Aged; D009367:Neoplasm Staging; D011379:Prognosis; D043244:Ribonuclease III / Q000235:genetics* / Q000378:metabolism; D000098830:AICDA (Activation-Induced Cytidine Deaminase)
chemical_list: C524942:MIRN155 microRNA, human; C543350:MIRN93 microRNA, human; D035683:MicroRNAs; C408087:DICER1 protein, human; C517918:DROSHA protein, human; D043244:Ribonuclease III; D000098830:AICDA (Activation-Induced Cytidine Deaminase); D003564:Cytidine Deaminase; D053487:DEAD-box RNA Helicases
keywords: AID; CLL; Dicer; Drosha; chronic lymphocytic leukemia