Zhen Shang

Tongji Hospital

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Jue Wang

Huazhong University of Science and Technology

Jianfeng Zhou

Xi’an Jiaotong-Liverpool University

Liang Huang

Huazhong University of Science and Technology

Tongjuan Li

Huazhong University of Science and Technology

Min Xiao

Huazhong University of Science and Technology

Yi Xiao

West China Hospital of Sichuan University

Chunrui Li

Chinese University of Hong Kong, Shenzhen

Lei Zhao

Tianjin University

Liting Chen

China Medical University

Jiaying Wu

Tongji Hospital

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Huazhong University of Science and Technology

116

Tongji Hospital

104

Chinese Academy of Sciences

Sun Yat-sen University

Shanghai Jiao Tong University

Hubei Provincial Center for Disease Control and Prevention

Chinese Academy of Medical Sciences & Peking Union Medical College

Sichuan University

University of Chinese Academy of Sciences

Zhejiang University

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TALENs-mediated gene disruption of FLT3 in leukemia cells: Using genome-editing approach for exploring the molecular basis of gene abnormality

Scientific Reports (2015)

Jue Wang Tongjuan Li Mi Zhou Zheng Hu Grace Zhou

Abstract Novel analytic tools are needed to elucidate the molecular basis of leukemia-relevant gene mutations in the post-genome era. We generated isogenic leukemia cell clones in which the FLT3 gene was disrupted in a single allele using TALENs. Isogenic clones with mono-allelic disrupted FLT3 were compared to an isogenic wild-type control clone and parental leukemia cells for transcriptional expression, downstream FLT3 signaling and proliferation capacity. The global gene expression profiles of mutant K562 clones and corresponding wild-type controls were compared using RNA- seq . The transcriptional levels and the ligand-dependent autophosphorylation of FLT3 were decreased in the mutant clones. TALENs-mediated FLT3 haplo-insufficiency impaired cell proliferation and colony formation in vitro . These inhibitory effects were maintained in vivo , improving the survival of NOD/SCID mice transplanted with mutant K562 clones. Cluster analysis revealed that the gene expression pattern of isogenic clones was determined by the FLT3 mutant status rather than the deviation among individual isogenic clones. Differentially expressed genes between the mutant and wild-type clones revealed an activation of nonsense-mediated decay pathway in mutant K562 clones as well as an inhibited FLT3 signaling. Our data support that this genome-editing approach is a robust and generally applicable platform to explore the molecular bases of gene mutations.

Abnormality

Chromosomal Abnormality

10.1038/srep18454

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Citations (12)

SLC39A6/ZIP6 is essential for zinc homeostasis and T-cell development in zebrafish

Biochemical and Biophysical Research Communications (2019)

Lei Zhao Jiaqi Tan Dan Li Lijun Jiang Tongjuan Li

Homeostasis

10.1016/j.bbrc.2019.02.148

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Citations (7)

Establishment of xenotransplantation model of human CN-AML with FLT3-ITD mut /NPM1 − in NOD/SCID mice

Journal of Huazhong University of Science and Technology [Medical Sciences] (2013)

Zhen Shang Jue Wang Di Wang Min Xiao Tongjuan Li

Xenotransplantation

NPM1

10.1007/s11596-013-1119-6

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Citations (1)

Study of immunophenotype of acute myeloid leukemia patients with NPM1 gene mutation

白血病·淋巴瘤 (2012)

Di Wang Min Xiao Li Zhu Zhe Geng Zhen Shang

Objective Toinvestigatetheimmunophenotypiccharacteristicsofacutemyeloidleukemia(AML) patients with NPM1 mutation. Methods The immunophenotype of 237 newly diagnosed AML patients were detected by flow cytometry. Real-time quantitative PCR was employed to detect the NPM1 mutation. The immunophenotype was then compared between the NPM1 mutated and wild type patients. Results The incidence of NPM1 mutation was 19.0 ％ (45/237) in all AML patients.The NPM1 mutated patients had lower expression of CD34,CD117,HLA-DR,CD15 and CD19 than the wild type patients(all P＜0.05).For AML patients with normal karyotype,the incidence of NPM1 mutation was 37.7 ％ (40/106),and the NPM1 mutated patients had lower expression of CD34,HLA-DR,CD15 and CD7 than the wild type patients(all P＜0.05).The NPM1 mutated patients with normal karyotype had lower expression of CD34 HLA-DR and CD7 in M1 subtype(all P ＜ 0.05); lower expression of HLA-DR and higher expression of CD9 in M2 subtype (all P ＜ 0.05) ; and lower expression of CD117 in M5 subtype compared with wild type patients (P ＜0.05). Conclusion The immunophenotypic characteristics of AML patients are changed by NPM1 mutation. The changes of immunophenotype varied in different FAB subtypes. Key words: Leukemia, nonlymphocytic, acute; Gene, NPM1; Immunophenotyping

NPM1

Immunophenotyping

CD117

10.3760/cma.j.issn.1009-9921.2012.04.001

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Corrigendum to “Human MLL-AF9 Overexpression Induces Aberrant Hematopoietic Expansion in Zebrafish”

BioMed Research International (2022)

Jiaqi Tan Lei Zhao Gaoxiang Wang Tongjuan Li Dan Li

[This corrects the article DOI: 10.1155/2018/6705842.].

10.1155/2022/9839650

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Aggressive NK-cell leukemia: clinical subtypes, molecular features, and treatment outcomes

Blood Cancer Journal (2017)

Yuting Tang D Wang Hui Luo Min Xiao H-S Zhou

Aggressive NK-cell leukemia (ANKL) is a rare form of NK cell neoplasm sporadically affecting people from Asia and Central and South America.The median overall survival (OS) is less than 2 months, irrespective of treatments.Epstein-Barr virus (EBV) is mostly detected in the leukemia cells and is proposed to contribute to the pathogenesis of ANKL [1][2][3] .ANKL represents a distinct disease entity within the continuous spectrum of EBV-associated T/NK-cell lymphoproliferative diseases (EBV-T/NK-LPDs).Patients with ANKL usually manifest a fulminant and extremely aggressive clinical course.However, some clinicopathologic features may be shared with different types of EBV-T/NK-LPDs, which leads to the occurrence of a few cases with features intermediate between two similar disorders 4-6 .The diagnosis of ANKL largely relies on the identification of morphologically and immunophenotypically aberrant leukemia cells 7 .Chromosomal gains and losses, activating STAT3 and STAT5 mutations, and HACE1 hypermethylation have only been sporadically detected [8][9][10] .Moreover, optimal therapy of ANKL has not yet been established 11 .To date, less than 350 cases of ANKL have been described in English literature worldwide.Because of the rarity of ANKL, the clinical features, potential pathogenesis, therapeutic strategies, and prognostic factors still lack in understanding.A multicenter

Hematology

10.1038/s41408-017-0021-z

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Citations (48)

Case report: Germline RECQL mutation potentially involved in hereditary predisposition to acute leukemia

Frontiers in Oncology (2023)

Wei Yuan Zhen Shang Kefeng Shen Qiuxia Yu Qiuxia Lv

The pathogenesis of acute leukemia is still complex and vague. Most types of acute leukemia are related to somatic gene mutations, and familial incidence is rare. Here we report a case of familial leukemia. The proband presented to our hospital with vaginal bleeding and disseminated intravascular coagulation at the age of 42 and was diagnosed with acute promyelocytic leukemia with typical PML-RARα fusion gene caused by t(15;17)(q24;q21) translocation. By taking the history, we found that the patient's second daughter had been diagnosed with B-cell acute leukemia with ETV6-RUNX1 fusion gene at age 6. Then we performed whole exome sequencing in peripheral blood mononuclear cells from these two patients at remission status and identified 8 shared germline gene mutations. Using functional annotation and Sanger sequencing validation, we finally focused on a single nucleotide variant in RecQ like helicase (RECQL), rs146924988, which was negative in the proband's healthy eldest daughter. This gene variant potentially led to a relative lack of RECQL protein, disordered DNA repair and chromatin rearrangement, which may mediate the occurrence of fusion genes, as driving factors for leukemia. This study identified a novel possible leukemia-related germline gene variant and provided a new understanding for the screening and pathogenesis of hereditary predisposition syndromes.

Hereditary Cancer

Genetic predisposition

10.3389/fonc.2023.1066083

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Citations (1)

Reports of Oncological Societies

Oncology Research and Treatment (2014)

Qiang Huo Chang Cai Qifeng Yang Xiaofang Geng Ji Ma

10.1159/000368687

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Citations (0)

Analysis of IKAROS6 expression in 73 patients with chronic myelogenous leukemia