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dc.contributor.authorÇetin, Deniz
dc.contributor.authorPektaş, Gökhan
dc.contributor.authorBozkurt, Gökay
dc.contributor.authorDöger, Füruzan Kacar
dc.contributor.authorYavaşoğlu, İrfan
dc.contributor.authorBolaman, Zahit
dc.contributor.authorKadıköylü, Gürhan
dc.date.accessioned2020-11-20T17:22:21Z
dc.date.available2020-11-20T17:22:21Z
dc.date.issued2020
dc.identifier.issn2148-8118
dc.identifier.issn2618-6020
dc.identifier.urihttps://app.trdizin.gov.tr//makale/TXpZMk5ETXdNQT09
dc.identifier.urihttps://hdl.handle.net/20.500.12809/7213
dc.description.abstractAurora 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.en_US
dc.item-language.isoengen_US
dc.item-rightsinfo:eu-repo/semantics/openAccessen_US
dc.titleHow is Aurora Kinase AExpression Altered in Chronic Lymphocytic Leukemia?en_US
dc.item-typearticleen_US
dc.contributor.departmenten_US
dc.contributor.departmentTempMuğla Sıtkı Koçman Üniversitesi Tıp Fakültesi İç Hastalıkları Anabilim Dalı, Muğla; Muğla Sıtkı Koçman Üniversitesi Tıp Fakültesi Hematoloji Anabilim Dalı, Muğla,Türkiye; Adnan Menderes Üniversitesi Tıp Fakültesi tıbbi Genetik Anabilim Dalı, Aydın,Türkiye; Adnan Menderes Üniversitesi Tıp Fakültesi Patoloji Anabilim Dalı, Aydın,Türkiye; Adnan Menderes Üniversitesi Tıp Fakültesi Hematoloji Anabilim Dalı, Aydın,Türkiye; Adnan Menderes Üniversitesi Tıp Fakültesi Hematoloji Anabilim Dalı, Aydın,Türkiye; Kent Hastanesi, Hematoloji Anabilim Dalı, İzmiren_US
dc.identifier.volume7en_US
dc.identifier.issue1en_US
dc.identifier.startpage24en_US
dc.identifier.endpage29en_US
dc.relation.journalMuğla Sıtkı Koçman Üniversitesi Tıp Dergisien_US
dc.relation.publicationcategoryMakale - Ulusal Hakemli Dergi - Kurum Öğretim Elemanen_US


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