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How is Aurora Kinase AExpression Altered in Chronic Lymphocytic Leukemia?

Date

2020

Author

Çetin, Deniz
Pektaş, Gökhan
Bozkurt, Gökay
Döger, Füruzan Kacar
Yavaşoğlu, İrfan
Bolaman, Zahit
Kadıköylü, Gürhan

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Abstract

Aurora kinase A is an enzyme which regulates the maturation and separation of centrosomes and the assembly and stability of mitotic spindles during mitosis. The dysregulation of Aurora kinase A is related with aneuploidy and a pronounced increase in cancerrisk. This study aims to determine how the expression of Aurora kinase A is altered in chronic lymphocytic leukemia (CLL). This prospective case-control study reviewed 41 patients who were newly diagnosed with CLL and 18 patients with benign hematologicaldiseases. Bone marrow aspiration and biopsy were performed in all patients. Aurora kinase A expression in bone marrow cells was assessed by quantitative reverse transcriptase-polymerase chain reaction. Bone marrow specimens were immunohistochemically stained for Aurora-A antibody. Chromosomal abnormalities including 13q deletion, 17p deletion and trisomy 12 were investigated by fluorescence in situ hybridization in bone marrow aspirates of CLL patients. The CLL patients and the patients with benign hematological diseases were statistically similar in aspect of Aurora kinase A mRNA expression through ?-actin and GAPDH housekeeping genes (respectively p=0.742 and p=0.229). Positive immunohistochemical staining for Aurora kinase A was significantly more frequent in CLL patients (p<0.001). Immunohistochemical staining for Aurora kinase A in bone marrow biopsies of CLL patients did not change significantly with respect to cytogenetic abnormalities such as 13q deletion, 17p deletion or trisomy 12 (p>0.05 for all).Aurora kinase A may play a role in the pathogenesis of CLL but this role may not be as evident as it has previously been specified.

Source

Muğla Sıtkı Koçman Üniversitesi Tıp Dergisi

Volume

7

Issue

1

URI

https://app.trdizin.gov.tr//makale/TXpZMk5ETXdNQT09
https://hdl.handle.net/20.500.12809/7213

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  • TR-Dizin İndeksli Yayınlar Koleksiyonu [3005]



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