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Downregulated stromal antigen 2 expression in de novo acute myeloid leukemia patients

The stromal antigen 2 (STAG2) gene encodes a component of the cohesin complex that participates in the regulation of sister chromatid separation during mitosis. When activated, STAG2 may act as a ‘caretaker’ tumor suppressor gene. As it is unknown whether STAG2 gene is responsible for the occurrence...

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Detalles Bibliográficos
Autores principales: Han, Qiaoyan, He, Xuefeng, Wu, Lili, Gao, Feng, Ye, Jinsong, Wu, Lingyu, Chen, Lu, Jiang, Xin, Sun, Miao, Chen, Suning
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5348667/
https://www.ncbi.nlm.nih.gov/pubmed/28352327
http://dx.doi.org/10.3892/etm.2017.4030
Descripción
Sumario:The stromal antigen 2 (STAG2) gene encodes a component of the cohesin complex that participates in the regulation of sister chromatid separation during mitosis. When activated, STAG2 may act as a ‘caretaker’ tumor suppressor gene. As it is unknown whether STAG2 gene is responsible for the occurrence and associated with the prognosis of acute myeloid leukemia (AML), the present study analyzed the relative expression levels of STAG2 in 127 de novo AML patients and 17 healthy volunteers using reverse transcription-quantitative polymerase chain reaction. In addition, AML patients were divided into three risk groups using cytogenetic and molecular genetic abnormalities to define their risk status. STAG2 gene expression was found to be significantly downregulated in de novo AML patients, when compared with the healthy controls; however, the expression was not significantly different in the various gender and age subgroups. Furthermore, no significant difference between risk groups was detected in AML patients. Thus, the STAG2 gene may serve an important role in AML development, but is not associated with prognosis in AML.