Clinical Study of SCIN Expression and Dromoter Methylation in Patients with Chronic Myeloid Leukemia.
- Author:
Zhi-Hui ZHANG
1
;
Xin-Yue LIAN
2
;
Xi-Xi LI
3
;
Ping-Fang HE
4
;
Jiang LIN
4
;
Jun QIAN
5
Author Information
- Publication Type:Journal Article
- MeSH: Blast Crisis; DNA Methylation; Down-Regulation; Fusion Proteins, bcr-abl; Gelsolin; genetics; Humans; Leukemia, Myelogenous, Chronic, BCR-ABL Positive; genetics; Promoter Regions, Genetic
- From: Journal of Experimental Hematology 2019;27(3):646-651
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To investigate the clinical significance of SCIN gene expression and promoter methylation in patients with chronic myeloid leukemia (CML).
METHODS:Real-time quantitative PCR was used to detect the expression level of SCIN in mononucleatr cells of bone marrow samples from 64 CML patients and 37 controls. The methylation levels of SCIN promoter in 65 patients with CML and 29 controls were detected by real-time quantitative methylation-specific PCR and bisulfite sequencing PCR.
RESULTS:The expression level of SCIN in CML patients was significantly down-regulated (P<0.05), compared with the control group. The down-regulation rate of SCIN expression in CML patients at chronic phase, accelerated phase and blast crisis was 61%, 67% and 75%, respectively. Spearman correlation analysis showed that the expression level of SCIN negatively correlated with the transcript level of BCR-ABL1 (R=-0.315, P<0.05). However, there was no significant difference in clinical parameters such as sex, age, white blood cell count, hemoglobin level, platelet count, chromosome, CML staging and BCL-ABL1 transcript level between low and high SCIN expression groups of CML patients (P>0.05). No significant difference in methylation of SCIN promoter between CML patients and controls, and no correlation between SCIN expression and promoter methylation were observed (P>0.05).
CONCLUSION:The SCIN expression is down-regulated in CML patients, which may relate with the pathogenesis that is, BCR-ABL1 fusion gene induces CML tumorigenesis. The down-regulation of SCIN expression may relate with the progression of CML.