Back to Search Start Over

TET2 rs2454206, TET2 rs12498609 and ASXL1 rs3746609 single nucleotide polymorphisms in patients with myelodysplastic syndromes.

Authors :
Hu, Jinjun
Xu, Jing
Tian, Tingting
Xie, Juan
Fan, Lifang
Zhu, Guiyang
Xia, Ting
Chen, Xi
Tan, Yanhong
Chen, Xiuhua
Ren, Fanggang
Zhang, Yaofang
Wang, Hongwei
Xu, Zhifang
Source :
Blood Cells, Molecules & Diseases. Feb2019, Vol. 74, p44-50. 7p.
Publication Year :
2019

Abstract

Abstract To study the association between TET2 rs2454206, TET2 rs12498609 and ASXL1 rs3746609 and Myelodysplastic syndromes (MDS), a total of 90 MDS patients and 143 healthy volunteers were included. The clinical data, bone marrow samples of patients and peripheral blood samples of volunteers were obtained. We found TET2 rs2454206 G/A genotype, TET2 rs12498609 G/C genotype and ASXL1 rs3746609 A/G genotype in 13.3%, 11.1%, 10.1% MDS patients and in 42.7%, 22.4%, 23.8% healthy volunteers (P < 0.001; P = 0.029; P = 0.009, respectively). TET2 rs2454206 G/A genotype was associated with higher serum LDH level in MDS (P = 0.025). Patients with TET2 rs12498609 G/C genotype were characterized with higher frequency of mutated SRSF2 gene (P = 0.042) and lower occurrence rate of anemia (P = 0.026) than those with C/C genotype. ASXL1 rs3746609 A/G genotype linked with higher thrombocyte counts (P = 0.02) and percent of total T lymphocyte (P = 0.029), whereas with lower percent of NK cell (P = 0.032) and B lymphocyte (P = 0.007). None of these three SNPs had impact on the overall survival and disease progression to AML. We concluded that People with TET rs2454206 G/A genotype, TET2 rs12498609 G/C genotype or ASXL1 rs3746609 A/G genotype were related to lower prevalence of MDS. All of the three SNPs were associated with certain laboratory features in MDS patients. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
10799796
Volume :
74
Database :
Academic Search Index
Journal :
Blood Cells, Molecules & Diseases
Publication Type :
Academic Journal
Accession number :
133068242
Full Text :
https://doi.org/10.1016/j.bcmd.2018.11.002