Zobrazeno 1 - 9
of 9
pro vyhledávání: '"Qiaoyang Ning"'
Autor:
Yonghui Li, Qiaoyang Ning, Jinlong Shi, Yang Chen, Mengmeng Jiang, Li Gao, Wenrong Huang, Yu Jing, Sai Huang, Anqi Liu, Zhirui Hu, Daihong Liu, Lili Wang, Clara Nervi, Yun Dai, Michael Q Zhang, Li Yu
Publikováno v:
EMBO Molecular Medicine, Vol 9, Iss 7, Pp 933-949 (2017)
Abstract DNA methylation patterns are frequently deregulated in t(8;21) acute myeloid leukaemia (AML), but little is known of the mechanisms by which specific gene sets become aberrantly methylated. Here, we found that the promoter DNA methylation si
Externí odkaz:
https://doaj.org/article/2979d31b2ba14c0488216e08649335d2
Autor:
Yushi Yao, Jihao Zhou, Lixin Wang, Xiaoning Gao, Qiaoyang Ning, Mengmeng Jiang, Jia Wang, Lili Wang, Li Yu
Publikováno v:
PLoS ONE, Vol 8, Iss 8, p e70522 (2013)
As one of the best known cancer testis antigens, PRAME is overexpressed exclusively in germ line tissues such as the testis as well as in a variety of solid and hematological malignant cells including acute myeloid leukemia. Therefore, PRAME has been
Externí odkaz:
https://doaj.org/article/724e7163716e4a3a91d36eb469398d68
Autor:
Hongliang Yang, Bing Xia, Chaoyu Wang, Yizhuo Zhang, Xiaofang Wang, Qiaoyang Ning, Yafei Wang, Yong Yu, Haifeng Zhao, Zhigang Zhao
Publikováno v:
Annals of Hematology. 97:453-457
We retrospectively analyzed a large study to investigate the association of hepatitis B virus (HBV) with aggressive B cell non-Hodgkin's lymphoma (aggressive B-NHL) in China, where HBV is endemic. HBV was present in 39 aggressive B-NHL patients (10.4
Autor:
Jinlong Shi, Mengmeng Jiang, Dai-Hong Liu, Li Yu, Anqi Liu, Sai Huang, Qiaoyang Ning, Li-Li Wang, Clara Nervi, Yang Chen, Yu Jing, Wenrong Huang, Michael Q. Zhang, Yun Dai, Yonghui Li, Zhirui Hu, Li Gao
Publikováno v:
EMBO Molecular Medicine. 9:933-949
DNA methylation patterns are frequently deregulated in t(8;21) acute myeloid leukaemia (AML), but little is known of the mechanisms by which specific gene sets become aberrantly methylated. Here, we found that the promoter DNA methylation signature o
Publikováno v:
Scientific Reports
SIRT2 is a member of the NAD+ dependent deacetylases. In this study, the associations between SIRT2 expression and molecular and clinical characteristics of patients with acute myeloid leukemia (AML) were evaluated by data from The Cancer Genome Atla
Autor:
Xiao-Ning Gao, Jinlong Shi, Yihan Xu, Ailing Deng, Na Shen, Y. Komeno, S. C. Wei, Yonghui Li, Clara Nervi, Fei Yan, Li Yu, Ji Lin, Xiao-Lin Lu, Jiuxia Pang, Dong-Er Zhang, Qiaoyang Ning, Li Gao, Shujun Liu
Publikováno v:
Leukemia, vol 29, iss 8
The mechanisms by which AML1/ETO (A/E) fusion protein induces leukemogenesis in acute myeloid leukemia (AML) without mutagenic events remain elusive. Here we show that interactions between A/E and hypoxia-inducible factor 1α (HIF1α) are sufficient
Autor:
Li-Li Wang, Li Yu, Yushi Yao, Mengmeng Jiang, Jia Wang, Jihao Zhou, Xiao-Ning Gao, Qiaoyang Ning, Lixin Wang
Publikováno v:
PLoS ONE, Vol 8, Iss 8, p e70522 (2013)
PLoS ONE
PLoS ONE
As one of the best known cancer testis antigens, PRAME is overexpressed exclusively in germ line tissues such as the testis as well as in a variety of solid and hematological malignant cells including acute myeloid leukemia. Therefore, PRAME has been
Autor:
Xiao-Ning Gao, Li-Li Wang, Ji Lin, Yonghui Li, Jihao Zhou, Yushi Yao, Qiaoyang Ning, Li Gao, Li Yu
Publikováno v:
PLoS ONE, Vol 8, Iss 2, p e55481 (2013)
PLoS ONE
PLoS ONE
AML1-ETO fusion protein (AE) is generated by t(8;21)(q22;q22) chromosomal translocation, which is one of the most frequently observed structural abnormalities in acute myeloid leukemia (AML) and displays a pivotal role in leukemogenesis. The histone
Autor:
Qiaoyang Ning, Shengcai Wei, Li Gao, Fei Yan, Jinlong Shi, Li Yu, Jiuxia Pang, Ailing Deng, Yihan Xu, Yonghui Li, Ji Lin, Xiaoning Gao, Shujun Liu, Xiao-Lin Lu, Na Shen
Publikováno v:
Blood. 124:3543-3543
The t(8;21)(q22;q22) translocation, resulting in a chimeric protein AML1/ETO (A/E), is one of the most common chromosomal abnormalities in acute myeloid leukemia (AML). It has been reported that additional mutagenic “hits” are required for A/E to