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CSF3R T618I, ASXL1 G942 fs and STAT5B N642H trimutation co-contribute to a rare chronic neutrophilic leukaemia manifested by rapidly progressive leucocytosis, severe infections, persistent fever and deep venous thrombosis.

作者信息

Luo Qianhui, Shen Jiankai, Yang Yuan, Tang Haiyan, Shi Meng, Liu Jun, Liu Zhonghua, Shi Xiaoliu, Yi Yan

机构信息

Department of Haematology, The Second Xiangya Hospital of Central South University, Changsha, Hunan Province, China.

Department of Medical Genetics, The Second Xiangya Hospital of Central South University, Changsha, Hunan Province, China.

出版信息

Br J Haematol. 2018 Mar;180(6):892-894. doi: 10.1111/bjh.14456. Epub 2016 Dec 16.

DOI:10.1111/bjh.14456
PMID:27984641
Abstract
摘要

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CSF3R T618I, ASXL1 G942 fs and STAT5B N642H trimutation co-contribute to a rare chronic neutrophilic leukaemia manifested by rapidly progressive leucocytosis, severe infections, persistent fever and deep venous thrombosis.CSF3R T618I、ASXL1 G942 fs和STAT5B N642H三联突变共同导致一种罕见的慢性嗜中性粒细胞白血病，其表现为快速进展的白细胞增多、严重感染、持续发热和深静脉血栓形成。
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T618I CSF3R mutations in chronic neutrophilic leukemia induce oncogenic signals through aberrant trafficking and constitutive phosphorylation of the O-glycosylated receptor form.T618I CSF3R 突变在慢性中性粒细胞白血病中通过异常转运和糖基化受体形式的组成性磷酸化诱导致癌信号。
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