25 results on '"Ke, Zhi-Yong"'
Search Results
2. Improved Outcome for Chinese Children With Acute Promyelocytic Leukemia: A Comparison of Two Protocols1
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Luo, Xue-Qun, Ke, Zhi-Yong, Huang, Li-Bin, Guan, Xiao-Qing, Zhang, Ying-Chuan, and Zhang, Xiao-Li
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- 2009
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3. High-risk childhood acute lymphoblastic leukemia in China: Factors influencing the treatment and outcome
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Luo, Xue-Qun, Ke, Zhi-Yong, Huang, Li-Bin, Guan, Xiao-Qing, Zhang, Ying-Chuan, and Zhang, Xiao-Li
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- 2009
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4. Maintenance Therapy With Dose-Adjusted 6-Mercaptopurine in Idiopathic Pulmonary Hemosiderosis
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Luo, Xue-Qun, Ke, Zhi-Yong, Huang, Li-Bin, Guan, Xiao-Qing, Zhang, Xiao-Li, Zhu, Jia, and Zhang, Ying-Chuang
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- 2008
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5. The Comparison of Outcome and Cost of Three Protocols for Childhood Non-High Risk Acute Lymphoblastic Leukemia in China
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Luo, Xue-Qun, Ke, Zhi-Yong, Guan, Xiao-Qing, Zhang, Ying-Chuang, Huang, Li-Bin, and Zhu, Jia
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- 2008
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6. Multicenter randomized trial of arsenic trioxide and Realgar‐Indigo naturalis formula in pediatric patients with acute promyelocytic leukemia: Interim results of the SCCLG‐APL clinical study.
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Yang, Ming‐Hua, Wan, Wu‐Qing, Luo, Jie‐Si, Zheng, Min‐Cui, Huang, Ke, Yang, Li‐Hua, Mai, Hui‐Rong, Li, Jian, Chen, Hui‐Qin, Sun, Xiao‐Fei, Liu, Ri‐Yang, Chen, Guo‐Hua, Feng, Xiaoqin, Ke, Zhi‐Yong, Li, Bin, Tang, Yan‐Lai, Huang, Li‐Bin, and Luo, Xue‐Qun
- Published
- 2018
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7. Obesity as the initial manifestation of central nervous system relapse of acute lymphoblastic leukemia: Case report and literature review
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Zhang, Li-Dan, Li, Yan-Hong, Ke, Zhi-Yong, Huang, Li-Bin, and Luo, Xue-Qun
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Obesity -- Diagnosis -- Care and treatment -- Case studies ,Acute lymphocytic leukemia -- Diagnosis -- Care and treatment -- Case studies ,Cerebrospinal fluid -- Properties ,Hypothalamus -- Physiological aspects ,Health - Abstract
Byline: Li-Dan. Zhang, Yan-Hong. Li, Zhi-Yong. Ke, Li-Bin. Huang, Xue-Qun. Luo A 6-year-old boy with acute lymphoblastic leukemia in remission experienced hyperphagia, obesity, and emotional disorders. Cytomorphologic examination of cerebral [...]
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- 2012
8. Arsenic trioxide and all-trans-retinoic acid selectively exert synergistic cytotoxicity against FLT3-ITD AML cells via co-inhibition of FLT3 signaling pathways.
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Wang, Li-Na, Tang, Yan-Lai, Zhang, Yin-Chuan, Zhang, Zu-Han, Liu, Xiao-Jian, Ke, Zhi-Yong, Li, Yu, Tan, Hui-Zhen, Huang, Li-Bin, and Luo, Xue-Qun
- Subjects
ARSENIC trioxide ,ACUTE myeloid leukemia treatment ,RETINOIC acid receptors ,LEUKEMIA ,CELL lines ,PROGNOSIS - Abstract
FLT3-ITD mutations occur in approximately 30% of acute myeloid leukemia (AML) and are associated with a poor outcome. Currently available FLT3 inhibitors havein vitrobut limited clinical activity in FLT3-ITD AML. Reports have shown that an arsenic trioxide (ATO)/all-trans-retinoic acid (ATRA) combination improves prognosis in acute promyelocytic leukemia, especially with FLT3-ITD, and ATO or ATRA alone enhances apoptosis in FLT3-ITD AML cells treated with FLT3 inhibitors, providing a rationale to investigate the role of ATO/ATRA in FLT3-ITD AML. Here, we demonstrate that an ATO/ATRA combination selectively exerts synergistic cytotoxicity against FLT3-ITD AML cell lines (MV4;11/MOLM-13). The signaling pathways affected by ATO/ATRA include FLT3/STAT5/MYC, FLT3/STAT5/E2F1, FLT3/ERK/ATF5 and FLT3/AKT/ATF5.ATF5 may function as an oncogene in FLT3-ITD AML. Our findings provide experimental evidence that supports further exploration of ATO/ATRA in FLT3-ITD AMLin vivoand warrants a clinical evaluation of regimens comprising an ATO/ATRA combination. [ABSTRACT FROM PUBLISHER]
- Published
- 2017
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9. Phospholipase C-gamma1 is required for cell survival in oxidative stress by protein kinase C
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Bai, Xiao-Chun, Deng, Fan, Liu, An-Ling, Zou, Zhi-Peng, Wang, Yu, Ke, Zhi-Yong, Ji, Qun-Sheng, and Luo, Shen-Qiu
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Mice, Knockout ,Mitogen-Activated Protein Kinase 1 ,Mitogen-Activated Protein Kinase 3 ,Caspase 3 ,Cell Survival ,Phospholipase C gamma ,Hydrogen Peroxide ,Enzyme Activation ,Isoenzymes ,Mice ,Oxidative Stress ,Proto-Oncogene Proteins c-bcl-2 ,Caspases ,Type C Phospholipases ,Animals ,Mitogen-Activated Protein Kinases ,Phosphorylation ,Cells, Cultured ,Protein Kinase C ,Research Article - Abstract
Phospholipase C-gamma1 (PLC-gamma1) activation has been reported to enhance cell survival during the cellular response to oxidative stress. We studied the role of protein kinase C (PKC) pathways in mediating PLC-gamma1 survival signalling in oxidative stress by using mouse embryonic fibroblasts genetically deficient in PLC-gamma1 (Plcg1(-/-)) and its wild type (Plcg1(+/+)). PLC-gamma1 was activated by H(2)O(2) treatment in a dose- and time-dependent manner. Activation of PKC was also markedly increased in both cell lines treated with H(2)O(2) (1-5 mM), but with low doses (50-200 microM), PKC activation was considerably decreased in Plcg1(-/-) cells. After treatment with H(2)O(2), PKC-dependent phosphorylation of Bcl-2 and cell viability of Plcg1(-/-) cells decreased dramatically and caspase-3-like activity increased significantly compared with that of the wild-type cells. Furthermore, pretreatment of Plcg1(+/+) cells with PKC-specific inhibitor decreased levels of PKC-dependent Bcl-2 phosphorylation, enhanced caspase-3 activity and their sensitivity to H(2)O(2). On the contrary, treatment of Plcg1(-/-) cells with PKC-specific activator increased the Bcl-2 phosphorylation, decreased caspase-3 activity and improved their survival. These results suggest that PLC-gamma1 mediates survival signalling in oxidative-stress response by PKC-dependent phosphorylation of Bcl-2 and inhibition of caspase-3.
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- 2002
10. Flavokawain B inhibits the growth of acute lymphoblastic leukemia cells via p53 and caspase-dependent mechanisms.
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Tang, Yan-Lai, Huang, Li-Bin, Tian, Yun, Wang, Li-Na, Zhang, Xiao-Li, Ke, Zhi-Yong, Deng, Wu-Guo, and Luo, Xue-Qun
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LYMPHOBLASTIC leukemia ,P53 antioncogene ,CASPASE inhibitors ,CELL proliferation ,APOPTOSIS ,PHARMACOLOGY - Abstract
The development of novel chemotherapeutic drugs is needed for the treatment of patients with acute lymphoblastic leukemia (ALL). In this study, the anti-leukemic effect and the potential molecular mechanisms of action of flavokawain B on ALL were investigated. Flavokawain B was found to significantly inhibit the cellular proliferation of B-ALL and T-ALL cell lines in a dose-dependent manner. It also induced cellular apoptosis by increasing the expression of p53, Bax and Puma, and activating the cleavage of caspase-3 and poly ADP-ribose polymerase (PARP). Furthermore, the enhancement of p53-dependent apoptosis by flavokawain B could be rescued by pifithrin-α, a pharmacological inhibitor of p53 transcriptional activity. Moreover, the proliferation of leukemia blast cells from 16 patients with ALL was inhibited by flavokawain B, and tumor growth in xenograft mice was also suppressed by this drug. In conclusion, our results demonstrate the therapeutic potential of flavokawain B for the treatment of ALL. [ABSTRACT FROM PUBLISHER]
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- 2015
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11. Five Chinese Pediatric Patients with Leukemias Possibly Arising from Immature Natural Killer Cells: Clinical Features and Courses.
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Guan, Xiao-Qing, Xu, Ling, Ke, Zhi-Yong, Huang, Li-Bin, Zhang, Xiao-Li, Zhang, Ying-Chuan, and Luo, Xue-Qun
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KILLER cells ,ACUTE leukemia ,PEDIATRIC therapy ,PEDIATRICS ,ANTINEOPLASTIC agents - Abstract
Leukemias arising from immature nature killer (NK) cells have been proposed as distinct entities and are rare. Treatment and prognosis of these diseases are controversial, and data on children are limited. According to the literature, one of these distinct leukemias may be myeloid/NK cell precursor acute leukemia (MNKPL), with the blasts being cytochemically myeloperoxidase negative (MPO
−− ) and phenotypically CD56++ CD3−− CD7++ CD34++ and myeloid antigens++ . The other may be myeloid/NK cell acute leukemia (MNKL), in which the blasts were cytochemically MPOdim and phenotypically CD56++ CD16−− CD3−− CD33++ HLA-DR−− . Between 2005 and 2008, 4 MNKPL and 1 MNKL children aged 1.3 to 12.5 years were encountered in the First Affiliated Hospital of Sun Yat-Sen University. In those with MNKPL, remarkable extramedullary involvement usually occurring in adults was not observed; however, myelofibrosis was found in 2 children. The child with MNKL abandoned treatment. Those with MNKPL were treated with a protocol designed for childhood high-risk acute lymphoblastic leukemia (ALL) containing cytarabine, mitoxantrone, etoposide, l-asparaginase, and methotrexate according to the myeloid and lymphoid characteristics of MNKPL. They responded slowly to chemotherapy and were in complete remission (CR) for 26 to 63 months, except 1 who died in CR from pneumonia. They had longer survival and seemed to have a better outcome than those reported previously. In conclusion, childhood leukemias with immature NK cell markers may have different characteristics from their adult counterparts. A protocol including agents used for acute myeloid leukemia combined with those for ALL is seemingly effective for treatment of MNKPL. However, a modified treatment strategy designed more specifically for MNKPL and longer observations are needed. [ABSTRACT FROM AUTHOR]- Published
- 2011
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12. A PROSPECTIVE STUDY OF FEBRILE EPISODES IN INPATIENT CHILDREN ON CHEMOTHERAPY.
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Ke, Zhi-Yong, Xu, Ling, Zhang, Ting-Ting, Mo, Ying-Lei, Huang, Li-Bin, Zhang, Xiao-Li, and Luo, Xue-Qun
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- 2010
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13. MiR-124 contributes to glucocorticoid resistance in acute lymphoblastic leukemia by promoting proliferation, inhibiting apoptosis and targeting the glucocorticoid receptor.
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Liang, Yan-Ni, Tang, Yan-Lai, Ke, Zhi-Yong, Chen, Yue-Qin, Luo, Xue-Qun, Zhang, Hua, and Huang, Li-Bin
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LYMPHOBLASTIC leukemia , *GLUCOCORTICOIDS , *BONE marrow diseases , *MICRORNA , *DRUG resistance , *THERAPEUTICS , *PREVENTION , *CANCER risk factors - Abstract
Acute lymphoblastic leukemia (ALL) is characterized by the accumulation of abnormal lymphoblasts in the bone marrow and blood. Though great progress has been made for improvement in clinical treatment during the past decades, some children with ALL still relapsed. Glucocorticoid (GC) resistance is an important clinical problem for ALL treatment failure. Therefore, further understanding of the mechanism of GC resistance and exploring novel therapeutic strategies are crucial for improving treatment outcome. The reported involvement of microRNAs (miRNAs) in drug resistance implied that deregulated miRNA expression might contribute to GC treatment response of ALL. However, individual miRNAs and their functional mechanisms potentially involved in the GC response are still largely unknown. In the present study, we found that miR-124 was up-regulated in prednisone insensitive human ALL cell line and prednisone-poor response ALL patients. Furthermore, it was found that miR-124 might contribute to GC resistance by promoting proliferation and inhibiting apoptosis of ALL cells. Importantly, we validated that miR-124, targeted and decreased the expression of glucocorticoid receptor (NR3C1), prevented the inhibitory effect of GC in ALL. These findings strongly suggest that miR-124 is critical in poor GC response and may serve as a potential therapeutic target in ALL with poor GC resistance. [ABSTRACT FROM AUTHOR]
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- 2017
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14. Melatonin inhibits MLL-rearranged leukemia via RBFOX3/hTERT and NF-κB/COX-2 signaling pathways.
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Tang, Yan-Lai, Sun, Xi, Huang, Li-Bin, Liu, Xiao-Jian, Qin, Ge, Wang, Li-Na, Zhang, Xiao-Li, Ke, Zhi-Yong, Luo, Jie-Si, Liang, Cong, Peng, Chun-Jin, Tang, Wen-Yan, Li, Yu, Huang, Wenlin, Luo, Xue-Qun, and Deng, Wuguo
- Abstract
MLL-rearranged leukemia is an aggressive malignancy associated with poor outcome, which is refractory to conventional treatment. Melatonin has been proven to exert anti-tumor activity, but the effect of melatonin on MLL-r leukemia and the underlying mechanism remain poorly understood. In this study, melatonin inhibited cell proliferation and induced apoptosis by activating the caspase-dependent apoptotic pathway in MLL-r leukemia cells. Mechanistic investigations revealed that melatonin suppressed the expression of hTERT by abrogating the binding activity of RBFOX3 to the hTERT promoter. Melatonin also blocked NF-κB nuclear translocation and suppressed NF-κB binding to the COX-2 promoter, thereby suppressing the expression of COX-2. In addition, clinical samples revealed that melatonin exerts anti-leukemic activity in primary MLL-r leukemia blasts ex vivo. In vivo, the mice treated with melatonin experienced a larger reduction in leukemic burden than the control group in a MLL-r leukemia xenograft mouse model. Collectively, these results suggest that melatonin inhibits MLL-rearranged leukemia through suppressing the RBFOX3/hTERT and NF-κB/COX-2 signaling pathways. Our findings provide new insights into the role of melatonin for MLL-r leukemia treatment. [ABSTRACT FROM AUTHOR]
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- 2019
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15. EFFECTS OF EARLY NUTRITION INTERVENTION ON IGF1, IGFBP3, INTESTINAL DEVELOPMENT, AND CATCH-UP GROWTH OF INTRAUTERINE GROWTH RETARDATION RATS.
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Qiu, Xiao-shan, Huang, Ting-ting, Deng, Hui-ying, Shen, Zhen-yu, Ke, Zhi-yong, Mei, Kai-yong, and Lai, Feng
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LABORATORY rats , *FETAL growth retardation , *BODY weight , *RATS , *HIGH-protein diet , *NUTRITION - Abstract
Objective To investigate the effects of early nutritional intervention on the serum insulin-like growth factor-1 (IGF1), insulin-like growth factor binding protein 3 (IGFBP3), intestinal development, and catch-up growth of intrauterine growth retardation (IUGR) rats by giving the IUGR new born rats different protein level diet. Methods IUGR rat model was built by starvation of pregnant female rats. Twenty-four IUGR pups and 8 normal pups were divided randomly into 4 groups: normal control group (C group); IUGR control group(S group), IUGR low-protein diet group (SL group), and IUGR high-protein diet group (SH group). Detected the serum IGF1, IGFBP3, body weight, body length, intestinal weight length, intestinal villi height (VH), crypt depth (CD), villi absorbing area (VSA), mucous thickness (MT), and disaccharidase at the 4th week. Results (1) The SH group showed the fastest catch-up growth, serum IGF1, IGFBP3, VH, and VSA were significantly higher than those of normal control group and IUGR control group. The intestinal weight and length, and the activities of lactase and saccharase, of the SH group also reached the normal control group level. (2) The SL group kept on small size, the serum IGF-1, IGFBP3, and most of intestinal histological indexes were all significantly lower than other groups. (3) IGF-1, IGFBP3 were positively correlated to intestinal VH, VSA, saccharase, body weight and length. Conclusions The serum IGF1 was a sensitive index to the catch-up growth. The early nutritional intervention of high-protein diet after birth is helpful for the catch-up growth of IUGR through promoting the intestinal development and the absorption of nutrition. [ABSTRACT FROM AUTHOR]
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- 2004
16. Intensive chemotherapy with dual induction and ALL-like consolidation for childhood acute myeloid leukemia: a respective report from multiple centers in China.
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Li JN, Chen YJ, Fan Z, Li QR, Liao LH, Ke ZY, Li Y, Wang LN, Yang CY, Luo XQ, Tang YL, Zhang XL, and Huang LB
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Background: Pediatric acute myeloid leukemia (AML) has poor prognosis and high rate of relapse and mortality, and exploration of new treatment options is still critically needed., Objectives: To summarize the outcome of our new treatment strategies for pediatric AML, which is characterized by dual induction and acute lymphoblastic leukemia (ALL) elements consolidation., Design: Retrospective, single-arm study., Methods: From July 2012 to December 2019, an intensive chemotherapy protocol was used for newly diagnosed children with AML, which contains dual induction, three courses of consolidations based on high-dose cytarabine, and two courses of consolidations composed of high-dose methotrexate, vincristine, asparaginase, and mercaptopurine (ALL-like elements). Blasts were monitored by bone marrow smears at intervals, and two lumbar punctures were performed during chemotherapy. We retrospectively analyzed the efficacy and safety of this study. The last follow-up was on 26 May 2023., Results: A total of 70 pediatric AMLs were included. The median age at diagnosis was 6.7 (0.5-16.0) years. The median initial WBC count was 23.74 × 10
9 /L, 11 of whom ⩾100 × 109 /L. After dual induction, there were 62 cases of complete remission (CR), 5 cases of partial remission, and 3 cases of nonremission. The CR rate was 88.57%. The median follow-up time was 5.8 (0.2-9.4) years, the 5-year overall survival was 78.2% ± 5%, the event-free survival (EFS) was 71.2% ± 5.6%, and the cumulative recurrence rate was 27.75%. The 5-year EFS of patients with initial WBC < 100 × 109 /L ( n = 59) and ⩾100 × 109 /L ( n = 11) were 76.4% ± 5.7% and 45.5% ± 15% ( p = 0.013), respectively. A total of 650 hospital infections occurred. The main causes of infection were respiratory tract infection (26.92%), septicemia (18.46%), stomatitis (11.85%), and skin and soft-tissue infection (10.46%)., Conclusion: This intensive treatment protocol with dual induction and ALL-like elements is effective and safe for childhood AML. Initial WBC ⩾ 100 × 109 /L was the only independent risk factor in this cohort., Trial Registration: It is a retrospective study, and no registration on ClinicalTrials.gov., Competing Interests: The authors declare that there is no conflict of interest., (© The Author(s), 2024.)- Published
- 2024
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17. Arsenic trioxide induces autophagic degradation of the FLT3-ITD mutated protein in FLT3-ITD acute myeloid leukemia cells.
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Liu XJ, Wang LN, Zhang ZH, Liang C, Li Y, Luo JS, Peng CJ, Zhang XL, Ke ZY, Huang LB, Tang YL, and Luo XQ
- Abstract
The prognosis of acute myeloid leukemia (AML) with FMS-like tyrosine kinase 3 internal tandem duplication (FLT3-ITD) mutations is poor. Some studies, including our previous study, have indicated that arsenic trioxide (ATO) exhibited significant anti-carcinogenic activity in FLT3-ITD AML cells and explored the possibility of targeting the FLT3-ITD protein for degradation as a therapy. Autophagy is a critical mechanism of the anti-leukemic effects of ATO. In this study, we explored the therapeutic efficacy of ATO treatment in a mouse model bearing FLT3-ITD AML and found that ATO significantly reduced the leukemic burden in bone marrow and spleen. We also found that autophagy was responsible for, at least in part, the degradation of the FLT3-ITD protein by ATO. After ATO treatment, MV4-11 cells showed complete autophagic flux. The autophagy inhibitor bafilomycin A or down-regulation of the key autophagy genes Atg5 and Atg7 reversed the FLT3 degradation induced by ATO. We also found that p62/SQSTM1 delivered FLT3-ITD proteins to the lysosome, where they were subsequently degraded. These results indicate that ATO can induce autophagic degradation of the FLT3-ITD mutated protein in FLT3-ITD AML., Competing Interests: Competing Interests: The authors have declared that no competing interest exists., (© The author(s).)
- Published
- 2020
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18. MTHFR-C677T Gene Polymorphism and Susceptibility to Acute Lymphoblastic Leukemia in Children: A Meta-Analysis.
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Li Y, Pei YX, Wang LN, Liang C, Tang YL, Zhang XL, Huang LB, Luo XQ, and Ke ZY
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- Genotype, Humans, Polymorphism, Single Nucleotide genetics, Precursor Cell Lymphoblastic Leukemia-Lymphoma pathology, White People genetics, Genetic Association Studies, Genetic Predisposition to Disease, Methylenetetrahydrofolate Reductase (NADPH2) genetics, Precursor Cell Lymphoblastic Leukemia-Lymphoma genetics
- Abstract
Background: The association between methylenetetrahydrofolate reductase (MTHFR) C677T polymorphism (rs1801133) and childhood acute lymphoblastic leukemia (ALL) is inconsistent., Objective: To explore the relationship between MTHFR-C677T polymorphism and susceptibility to childhood ALL., Methods: PubMed, EMBASE, Web of Science, CNKI, Wanfang, VIP, and other databases were searched from the establishment of the database to November 2019, and all the case-control studies that met the inclusion criteria were collected. Stata 15.0 was used for meta-analysis, with calculation of the odds ratio (OR) of the relationship between MTHFR-C677T polymorphism and childhood ALL susceptibility. Ethnicity was analyzed by subgroup analysis., Results: A total of 26 studies were included in this meta-analysis, including 4,682 children with ALL and 7144 controls. The results showed that there was no significant difference in the comparison of population of allele model, dominant gene model, recessive gene model, homozygous gene model, heterozygous gene model, and the comparison of Caucasian children. The results of the Asian child analysis suggested that the combined OR of the dominant gene model (CC + CT versus TT), homozygous model (CC versus TT) and heterozygous model (CT versus TT) was 1.32 (95% confidence interval [CI]: 1.03-1.70), 1.37 (95% CI: 1.02-1.84), and 1.27 (95% CI: 1.01-1.59), respectively, with statistically significant differences. However, there was no significant difference between the allele model and recessive gene model among Asian children., Conclusion: The MTHFR C677T polymorphism is related to ALL in children, especially in Asian children. CC + CT, CC, and CT genotypes can increase the risk of ALL, but no association has been found in Caucasian children.
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- 2020
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19. Butein inhibits cell proliferation and induces cell cycle arrest in acute lymphoblastic leukemia via FOXO3a/p27kip1 pathway.
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Tang YL, Huang LB, Lin WH, Wang LN, Tian Y, Shi D, Wang J, Qin G, Li A, Liang YN, Zhou HJ, Ke ZY, Huang W, Deng W, and Luo XQ
- Subjects
- Cell Cycle Checkpoints drug effects, Cell Proliferation drug effects, Child, Child, Preschool, Female, Humans, Male, Precursor Cell Lymphoblastic Leukemia-Lymphoma genetics, Precursor Cell Lymphoblastic Leukemia-Lymphoma metabolism, Precursor Cell Lymphoblastic Leukemia-Lymphoma pathology, Signal Transduction drug effects, Chalcones pharmacology, Cyclin-Dependent Kinase Inhibitor p27 metabolism, Forkhead Box Protein O3 metabolism, Precursor Cell Lymphoblastic Leukemia-Lymphoma drug therapy
- Abstract
Acute lymphoblastic leukemia (ALL) is a common hematological malignancy characterized by the uncontrolled proliferation of leukemia cells in children. Discovering and developing effective chemotherapeutic drugs are needed for ALL. In this study, we investigated the anti-leukemic activity of butein and its action mechanisms in ALL. Butein was found to significantly suppress the cellular proliferation of ALL cell lines and primary ALL blasts in a dose-dependent manner. It also induced cell cycle arrest by decreasing the expression of cyclin E and CDK2. We also found that butein promoted nuclear Forkhead Class box O3a (FOXO3a) localization, enhanced the binding of FOXO3a on the p27kip1 gene promoter and then increased the expression of p27kip1. Moreover, we showed that FOXO3a knockdown significantly decreased the proliferation inhibition by butein, whereas overexpression of FOXO3a enhanced the butein-mediated proliferation inhibition. However, overexpression of FOXO3a mutation (C-terminally truncated FOXO3a DNA-binding domain) decreased the proliferation inhibition by butein through decreasing the expression of p27kip1. Our results therefore demonstrate the therapeutic potential of butein for ALL via FOXO3a/p27kip1 pathway.
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- 2016
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20. Mandibuloacral dysplasia type A-associated progeria caused by homozygous LMNA mutation in a family from Southern China.
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Luo DQ, Wang XZ, Meng Y, He DY, Chen YM, Ke ZY, Yan M, Huang Y, and Chen DF
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- Asian People genetics, Child, Child, Preschool, China, Female, Humans, Infant, Male, Osteolysis genetics, Pedigree, Rare Diseases genetics, Siblings, Acro-Osteolysis genetics, Homozygote, Lamin Type A genetics, Lipodystrophy genetics, Mandible abnormalities, Mutation, Progeria genetics
- Abstract
Background: Mandibuloacral dysplasia type A (MADA) is a rare autosomal recessive disorder, characterized by growth retardation, skeletal abnormality with progressive osteolysis of the distal phalanges and clavicles, craniofacial anomalies with mandibular hypoplasia, lipodystrophy and mottled cutaneous pigmentation. Some patients may show progeroid features. MADA with partial lipodystrophy, more marked acral, can be caused by homozygous or compound heterozygous mutation in the gene encoding lamin A and lamin C (LMNA). MADA and Hutchinson-Gilford progeria syndrome are caused by the same gene and may represent a single disorder with varying degrees of severity. MAD patients characterized by generalized lipodystrophy (type B) affecting the face as well as extremities and severe progressive glomerulopathy present heterozygous compound mutations in the ZMPSTE24 gene., Cases Presentations: We described a rare pedigree from Southern China, among them all three children presented with phenotypes of MADA associated progeria. The two elder sisters had developed severe mandibular hypoplasia associated progeria since the age of 1 year. The eldest sister showed a progressive osteolysis. The youngest son of 10 months showed severer lesions than those of his sisters at the same age, and presented possible muscle damage, and his symptoms progressed gradually. Three genes mutations including LMNA, ZMPSTE24 and BANF1 were tested in the family. LMNA gene sequencing revealed a homozygous missense mutation, c.1579C > T, p.R527C for all three siblings, and heterozygous mutations for their parents, whereas no mutations of ZMPSTE24 and BANF1 genes was detected among them., Conclusions: The same homozygous mutation of c.1579C > T of LMNA gene led to MADA associated progeria for the present family. The course of osteolysis for MADA is progressive.
- Published
- 2014
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21. Genome-wide analysis of small RNA and novel MicroRNA discovery in human acute lymphoblastic leukemia based on extensive sequencing approach.
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Zhang H, Yang JH, Zheng YS, Zhang P, Chen X, Wu J, Xu L, Luo XQ, Ke ZY, Zhou H, Qu LH, and Chen YQ
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- Bone Marrow metabolism, Computational Biology, Gene Library, Genome, Genome-Wide Association Study, Humans, Models, Biological, Models, Genetic, Recurrence, Reverse Transcriptase Polymerase Chain Reaction, Gene Expression Regulation, Leukemic, MicroRNAs genetics, Precursor Cell Lymphoblastic Leukemia-Lymphoma genetics, Precursor Cell Lymphoblastic Leukemia-Lymphoma metabolism, RNA genetics, Sequence Analysis, DNA
- Abstract
Background: MicroRNAs (miRNAs) have been proved to play an important role in various cellular processes and function as tumor suppressors or oncogenes in cancers including leukemia. The identification of a large number of novel miRNAs and other small regulatory RNAs will provide valuable insights into the roles they play in tumorgenesis., Methodology/principal Findings: To gain further understanding of the role of miRNAs relevant to acute lymphoblastic leukemia (ALL), we employed the sequencing-by-synthesis (SBS) strategy to sequence small RNA libraries prepared from ALL patients and normal donors. In total we identified 159 novel miRNAs and 116 novel miRNA*s from both libraries. Among the 159 novel miRNAs, 42 were identified with high stringency in our data set. Furthermore, we demonstrated the different expression patterns of 20 newly identified and several known miRNAs between ALL patients and normal donors, suggesting these miRNAs may be associated with ALL and could constitute an ALL-specific miRNA signature. Interestingly, GO "biological process" classifications revealed that a set of significantly abnormally expressed miRNAs are associated with disease relapse, which implies that these dysregulated miRNAs might promote the progression of ALL by regulating genes involved in the pathway of the disease development., Conclusion/significance: The study presents a comprehensive picture of the expression of small RNAs in human acute lymphoblastic leukemia and highlights novel and known miRNAs differentially expressed between ALL patients and normal donors. To our knowledge, this is the first study to look at genome-wide known and novel miRNA expression patterns in in human acute lymphoblastic leukemia. Our data revealed that these deregulated miRNAs may be associated with ALL or the onset of relapse.
- Published
- 2009
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22. High-dose chemotherapy without stem cell transplantation for refractory childhood systemic lupus erythematosus.
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Luo XQ, Mo Y, Ke ZY, Xu L, Jiang XY, Zhang TT, and Chen SM
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- Adolescent, Child, Dose-Response Relationship, Drug, Female, Follow-Up Studies, Humans, Stem Cell Transplantation, Lupus Erythematosus, Systemic drug therapy
- Abstract
Background: Intensive chemotherapy followed by autologous hematopoietic stem cell transplantation (ASCT) is effective for refractory systemic lupus erythematosus (SLE). When intensive chemotherapy is immunoablative but nonmyeloablative, ASCT for hematopoietic reconstitution, with the risk of reinfusing autoreactive lymphocytes, is unnecessary., Methods: Four children aged 12-16 years were enrolled, 3 with WHO class IV nephritis, 2 with hemolytic anemia and 1 with thrombocytopenia. Median disease duration prior to the study was 4 years (range 1-6). Previous therapy, including intravenous bolus cyclophosphamide (Cy) with a median accumulated dose of 6.5 g/m(2) and high-dose methylprednisolone with a median accumulated dose of 370 mg/kg, had failed. The protocol included: Cy 1.2 g/m(2) daily for 4 days, fludarabine 30 mg/m(2) daily for 4 days, porcine antilymphocyte globulin 25 mg/kg daily for 3 days., Results: Themedian duration of absolute neutrophil count <0.5 x 10(9)/l was 5.5 days after treatment. The median SLE Disease Activity Index and urine protein decreased from 8.5 and 3.4 to 1.0 and 0.1 g/day at the date of last follow-up (median 20 months), respectively. Two cases with hemolytic anemia and 1 with thrombocytopenia before treatment recovered to normal or near normal hemogram, respectively. All patients achieved complete or partial remission within 10-28 months of follow-up., Conclusion: Intensive chemotherapy leads to rapid hematopoietic reconstitution without ASCT and appears beneficial in refractory childhood SLE. Further study is needed., (2008 S. Karger AG, Basel.)
- Published
- 2008
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23. Effect of early nutrition on intestine development of intrauterine growth retardation in rats and its correlation to leptin.
- Author
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Qiu XS, Huang TT, Shen ZY, Deng HY, and Ke ZY
- Subjects
- Animals, Dietary Proteins pharmacology, Disease Models, Animal, Female, Fetal Growth Retardation blood, Fetal Nutrition Disorders blood, Male, Pregnancy, Rats, Rats, Sprague-Dawley, Fetal Growth Retardation diet therapy, Fetal Growth Retardation physiopathology, Fetal Nutrition Disorders diet therapy, Fetal Nutrition Disorders physiopathology, Intestines embryology, Leptin blood
- Abstract
Aim: To investigate the intestine and body development of intrauterine growth retardation (IUGR) rats under early different protein diet and to analyze the correlation between leptin and intestine and body development., Methods: An IUGR rat model was established by food restriction of pregnant female rats. Fifty-six neonatal IUGR rats and 24 neonatal normal rats were randomly divided into normal control group (C group), IUGR model group (SC group), low protein diet IUGR group (SL group), and high protein diet IUGR group (SH group). Eight rats were killed per group at wk 0, 4, and 12. Serum leptin, body weight (BW), body length (BL), intestinal weight (IW), intestinal length (IL), and intestinal disaccharidase (including lactase, maltase, and saccharase) were detected., Results: BW (4.50+/-0.41 g), BL (5.96+/-0.40 cm), IW (0.05+/-0.01 g), and IL (15.9+/-2.8 cm) in neonatal IUGR rats were much lower than those in C group (6.01+/-0.55 g, 6.26+/-0.44 cm, 0.10+/-0.02 g, 21.8+/-2.7 cm, P<0.05), while intestinal lactase and maltase activities were higher than those in C group. SH group showed the fastest catch up growth and their BW, BL, IW, and IL reached the C group level at wk 4. SC group showed relatively slower catch up growth than SH group, and their BW, BL, IW did not reach the C group level at wk 4. SL group did not show intestine and body catch up growth. Intestinal maltase (344+/-33 micromol/(min.g)) and saccharase activities (138+/-32 micromol/(min.g)) in SL group were both markedly lower than those in C group (751+/-102, 258+/-27 micromol/(min.g), P<0.05). There were no significant differences in lactase activities at wk 4 and disaccharidase activities at wk 12 among all groups (P>0.05). The leptin level in SL group (0.58+/-0.12 ng/mL) was the highest in all groups, and much lower in SH group (0.21+/-0.03 ng/mL) than that in any other IUGR groups at wk 4 (P<0.05). Leptin was negatively related to BW (r = -0.556, P = 0.001), IW (r = -0.692, P = 0.001) and IL (r = -0.738, P = 0.000) at wk 4, while no correlation was found at wk 12., Conclusion: High protein diet is a reasonable early nutritional mode to IUGR rats in promoting intestine and body catch up growth.
- Published
- 2005
- Full Text
- View/download PDF
24. Antisense epidermal growth factor receptor (EGFR) transfection down-regulates EGFR expression and suppresses the malignant phenotype of human nasopharyngeal carcinoma CNE-2 cell line.
- Author
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Deng F, Wang Y, Zeng FY, Zou ZP, Bai XC, Lu D, Ke ZY, and Luo SQ
- Subjects
- Animals, Cell Division, Cell Line, Tumor, Down-Regulation, ErbB Receptors genetics, Female, Humans, Mice, Nasopharyngeal Neoplasms etiology, Nasopharyngeal Neoplasms pathology, Phenotype, Transfection, ErbB Receptors antagonists & inhibitors, Nasopharyngeal Neoplasms therapy, RNA, Antisense therapeutic use
- Abstract
Objective: To determine whether epidermal growth factor receptor (EGFR) expression contributes to tumor growth of poorly differentiated human nasopharyngeal carcinoma CNE-2 cell lines., Methods: An expression vector containing a N-terminal fragment (1.35 kb) of human EGFR in the antisense orientation was transfected into CNE-2 cell lines via lipofectamine. The established clones resistant to G418 were isolated and characterized, and the tumor-inhibiting effect of antisense EGFR expression was evaluated in terms of tumor growth and metastasis at different time after subcutaneous inoculation into nude mice., Results: Down-regulated EGFR expression in the cells with antisense vector transfection was demonstrated by ligand binding assay. The growth rate and the ability to grow in soft agarose of these antisense transfectants were also reduced. After inoculation into nude mice, EGFR antisense transfectants showed a longer latency period, slower tumor growth and lower metastatic rates to the lymph nodes and lung in comparison with the parental cells., Conclusions: These results suggest that these EGFR antisense cDNA-transfected CNE-2 cells are of value to further delineate the role of EGFR in the development and progression of nasopharyngeal carcinoma.
- Published
- 2003
25. Phospholipase C-gamma1 is required for cell survival in oxidative stress by protein kinase C.
- Author
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Bai XC, Deng F, Liu AL, Zou ZP, Wang Y, Ke ZY, Ji QS, and Luo SQ
- Subjects
- Animals, Caspase 3, Caspases metabolism, Cell Survival drug effects, Cells, Cultured, Enzyme Activation drug effects, Hydrogen Peroxide toxicity, Isoenzymes deficiency, Isoenzymes genetics, Mice, Mice, Knockout, Mitogen-Activated Protein Kinase 1 metabolism, Mitogen-Activated Protein Kinase 3, Mitogen-Activated Protein Kinases metabolism, Oxidative Stress drug effects, Phospholipase C gamma, Phosphorylation, Proto-Oncogene Proteins c-bcl-2 metabolism, Type C Phospholipases deficiency, Type C Phospholipases genetics, Cell Survival physiology, Isoenzymes metabolism, Oxidative Stress physiology, Protein Kinase C metabolism, Type C Phospholipases metabolism
- Abstract
Phospholipase C-gamma1 (PLC-gamma1) activation has been reported to enhance cell survival during the cellular response to oxidative stress. We studied the role of protein kinase C (PKC) pathways in mediating PLC-gamma1 survival signalling in oxidative stress by using mouse embryonic fibroblasts genetically deficient in PLC-gamma1 (Plcg1(-/-)) and its wild type (Plcg1(+/+)). PLC-gamma1 was activated by H(2)O(2) treatment in a dose- and time-dependent manner. Activation of PKC was also markedly increased in both cell lines treated with H(2)O(2) (1-5 mM), but with low doses (50-200 microM), PKC activation was considerably decreased in Plcg1(-/-) cells. After treatment with H(2)O(2), PKC-dependent phosphorylation of Bcl-2 and cell viability of Plcg1(-/-) cells decreased dramatically and caspase-3-like activity increased significantly compared with that of the wild-type cells. Furthermore, pretreatment of Plcg1(+/+) cells with PKC-specific inhibitor decreased levels of PKC-dependent Bcl-2 phosphorylation, enhanced caspase-3 activity and their sensitivity to H(2)O(2). On the contrary, treatment of Plcg1(-/-) cells with PKC-specific activator increased the Bcl-2 phosphorylation, decreased caspase-3 activity and improved their survival. These results suggest that PLC-gamma1 mediates survival signalling in oxidative-stress response by PKC-dependent phosphorylation of Bcl-2 and inhibition of caspase-3.
- Published
- 2002
- Full Text
- View/download PDF
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