Volume 8, Issue 1 (1-2018)                   Iran J Ped Hematol Oncol 2018, 8(1): 54-61 | Back to browse issues page

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Ayatollahi H, Keshavarzi A, Shams B, Barzegar M, Amirpour M, Sheikhi M, et al . Relationship Between SOX17 Gene Expression and Prognosis in Acute Myeloid Leukemia. Iran J Ped Hematol Oncol. 2018; 8 (1) :54-61
URL: http://ijpho.ssu.ac.ir/article-1-312-en.html
Cancer Molecular Pathology Research Center, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
Abstract:   (953 Views)
Background: Acute Myeloid Leukemia (AML) is a group of heterogeneous malignancies caused by defects in differentiation of hematopoietic cells. SRY-box containing gene 17(SOX17) is a transcription factor which plays an important role in several biological processes, including cardiogenesis, angiogenesis, and lymphopoiesis. Aberrant expression of SOX17 has been detected in solid tumors. This study was performed to investigate the alternations of SOX17 expression in AML patients.
Materials and methods: This case-control study included 54 AML patients who were referred to Molecular Pathology Cancer Research Center of Ghaem Hospital in North East of Iran from October 2011 to May 2016. Patients were classified according to French-American-British (FAB) and World Health Organization (WHO) criteria. RNA was extracted from peripheral blood. SOX17 gene expression was evaluated by real-time quantitative polymerase chain reaction (RQ-PCR).
Results: Over expression of SOX17 was observed in 34 (62.96%) AML  patients. No relation was noticed between SOX17 expression and patient survival (p=0.493). In addition, no correlation among patient survival, Sex(p=0.322),hemoglobin(p=0.866) and white blood cell (WBC) (p=0.103).
Conclusion: Based on these results, SOX17 did not have any important role in AML pathogenesis. Thus, it can’t be used as a diagnostic and prognostic factor. However, more studies are required to fully elucidate the role of SOX17 in AML.

Full-Text [PDF 227 kb]   (217 Downloads)    
Type of Study: Research | Subject: Special
Received: 2017/06/22 | Accepted: 2017/09/27 | Published: 2017/12/11

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