期刊论文

Nie, Ling;Zhang, Ji

英文

BLOOD CELLS MOLECULES AND DISEASES

1079-9796

2020

85

102477

10.1016/j.bcmd.2020.102477

This work was funded by the National Natural Science Foundation of China (nos. 81870105 and 81770107), Key Project of Science and Technology of Hunan Provincial Health Commission (no. 20201921) and the National Key Research and Development Program of China (2018YFA0107800), the postgraduate innovation project of Central South University (2016zzts165) and the graduate student innovation project of Central South University (2017zzts353). CRediT authorship contribution statement Yijin Kuang:Investigation, Data curation, Writing - original draft.Xu Han:Conceptualization, Methodology, Software.Pengfei Cao:Resources, Visualization, Investigation.Dehui Xiong:Writing - original draft.Yuanliang Peng:Data curation.Zhaoping Liu:Methodology, Software.Zhenru Xu:Investigation.Long Liang:Software, Validation.Mridul Roy:Writing - review & editing.Jing Liu:Supervision, Writing - review & editing.Ling Nie:Formal analysis, Investigation.Ji Zhang:acquisition, Conceptualization,

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Chronic myeloid leukemia (CML) is a kind of myeloproliferative disorder caused by a constitutively active BCR-ABL tyrosine kinase. Tyrosine kinase inhibitors (TKIs), imatinib and its derivatives, have achieved great progress in the treatment of CML. However, many CML patients do not respond to TKIs alone. p19(INK4d), a cyclin-dependent kinase inhibitor, plays important roles in proliferation, DNA damage repair, apoptosis and cell differentiation, but its role in CML is unknown. Herein, we found that the expression of p19(INK4d) in CML patients was significantly lower than that in healthy contr...