Kronik Lenfositik Lösemide Aurora Kinaz A Ekspresyonu Değişikliği

Year 2020, Volume: 7 Issue: 1, 24 - 29, 28.04.2020

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

Abstract

Aurora kinaz A, sentrozomların olgunlaşması ve ayrılmasını, mitoz sırasında iğ ipliklerinin oluşumu ve stabilitesini düzenleyen bir enzimdir. Aurora kinaz A’nın düzensizliği anöploidi ve kanser riskinde belirgin artış ile ilişkilidir. Bu çalışma, Aurora kinaz A ekspresyonunun kronik lenfositik lösemide (KLL) nasıl değiştiğini belirlemeyi amaçlamaktadır. Bu prospektif olgu-kontrol çalışmasında yeni tanı konmuş 41 KLL hastası ve benign hematolojik hastalıklara sahip 18 hasta değerlendirildi. Tüm hastalara kemik iliği aspirasyon ve biyopsisi uygulandı. Kemik iliği hücrelerinde Aurora kinaz A ekspresyonu, kantitatif ters transkriptaz-polimeraz zincir reaksiyonu ile belirlendi. Kemik iliği kesitleri immunhistokimyasal olarak Aurora-A antikoru için boyandı. KLL hastalarının kemik iliği aspiratlarında floresans insitu hibridizasyon yöntemiyle 13q delesyonu, 17p delesyonu ve trizomi 12 kromozom anomalileri araştırıldı. KLL hastaları ve benign hematolojik hastalığı olan hastalar, Aurora kinaz A mRNA ekspresyonu açısından istatistiksel olarak benzerdi (β-actin ve GAPDH housekeeping genleri için sırasıyla p=0.742 ve p=0.229). Aurora kinaz A için pozitif immunhistokimyasal boyanma KLL hastalarında anlamlı olarak daha sıktı (p<0.001). KLL hastalarının kemik iliği biyopsilerinde Aurora kinaz A immunhistokimyasal boyanması açısından, 13q delesyonu, 17p delesyonu veya trizomi 12 gibi sitogenetik anormaliklerle ilgili anlamlı farklılık gözlenmedi (p>0.05 her biri için). Aurora kinaz A, KLL patogenezinde rol oynayabilir ancak bu rol daha önce belirtildiği kadar belirgin olmayabilir.

Keywords

Aurora Kinaz A, Kemik Iliği, Kronik Lenfositik Lösemi

Supporting Institution

Adnan Menderes Üniversitesi Bilimsel Araştırma Projeleri Birimi

Project Number

TPF-13009

How is Aurora Kinase A Expression Altered in Chronic Lymphocytic Leukemia?

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 cancer risk. 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 hematological diseases. 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 β-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.

Keywords

Aurora Kinase A, Bone Marrow, Chronic Lymphocytic Leukemia

Project Number

TPF-13009

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