Beta-catenin and cyclin D1 mRNA levels in newly diagnosed patients with acute myeloid leukemia and their significance.
- Author:
Yun-Xiu WANG
1
;
Ji-Hong ZHANG
;
Zhao-Wei GU
Author Information
1. China Medical University, Shengjing Hospital, Shenyang 110022, Liaoning Province, China.
- Publication Type:Journal Article
- MeSH:
Adult;
Cyclin D1;
metabolism;
Female;
Humans;
Leukemia, Myeloid, Acute;
genetics;
metabolism;
Male;
RNA, Messenger;
metabolism;
Signal Transduction;
Young Adult;
beta Catenin;
genetics;
metabolism
- From:
Journal of Experimental Hematology
2009;17(2):304-308
- CountryChina
- Language:Chinese
-
Abstract:
This study was aimed to quantitatively detect the levels of beta-catenin and cyclin D1 mRNA in various subgroups of acute myeloid leukemia (AML) and to analyze their potential relationship, so as to provide theoretical basis for exploring the role of Wnt/beta-catenin pathway in the pathogenesis of AML. Real time fluorescent quantitative RT-PCR was used to detect the relative expression levels of beta-catenin and cyclin D1 mRNA, to analyze changes of the two gene expressions and their relationship. The results showed that the beta-catenin mRNA expression level in BMMNC of AML patients was significantly higher than that in benign blood disease patients (p < 0.05), but no statistical difference was found among the various subgroups of AML (p > 0.05). In AML there was overexpression of cyclin D1 mRNA, and its expression level was significantly higher than that in benign blood disease group (p < 0.05), but there was no statistical difference among the subtypes of AML. The expression levels of beta-catenin and cyclin D1 were correlated each other in AML-M(1), M(2) and M(4) (r values were 0.822, 0.627, 0.712 respectively; p values were 0.001, 0.020, 0.002 respectively). It is concluded that the over-expressions of beta-catenin and cyclin D1 exit in AML patients, and the significant correlation appears in part of the subgroups, which means that the Wnt/beta-catenin pathway is aberrantly activated in AML, probably activating the downstream target gene cyclin D1 and participating in the regulation of cell cycle disturbance and abnormal proliferation of leukemic cells.
