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38 results on '"Tang, Qiuqiong"'

2. Supplementary Table S1 from Lisaftoclax in Combination with Alrizomadlin Overcomes Venetoclax Resistance in Acute Myeloid Leukemia and Acute Lymphoblastic Leukemia: Preclinical Studies

Author

Zhai, Yifan, primary, Tang, Qiuqiong, primary, Fang, Douglas D., primary, Deng, Jing, primary, Zhang, Kaixiang, primary, Wang, Qixin, primary, Yin, Yan, primary, Fu, Chengcheng, primary, Xue, Sheng-Li, primary, Li, Na, primary, Zhou, Feng, primary, and Yang, Dajun, primary

Published
2023
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3. Supplementary Figures S1-S5 from Lisaftoclax in Combination with Alrizomadlin Overcomes Venetoclax Resistance in Acute Myeloid Leukemia and Acute Lymphoblastic Leukemia: Preclinical Studies

Author

Zhai, Yifan, primary, Tang, Qiuqiong, primary, Fang, Douglas D., primary, Deng, Jing, primary, Zhang, Kaixiang, primary, Wang, Qixin, primary, Yin, Yan, primary, Fu, Chengcheng, primary, Xue, Sheng-Li, primary, Li, Na, primary, Zhou, Feng, primary, and Yang, Dajun, primary

Published
2023
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4. Supplementary Appendix 1 from Lisaftoclax in Combination with Alrizomadlin Overcomes Venetoclax Resistance in Acute Myeloid Leukemia and Acute Lymphoblastic Leukemia: Preclinical Studies

Author

Zhai, Yifan, primary, Tang, Qiuqiong, primary, Fang, Douglas D., primary, Deng, Jing, primary, Zhang, Kaixiang, primary, Wang, Qixin, primary, Yin, Yan, primary, Fu, Chengcheng, primary, Xue, Sheng-Li, primary, Li, Na, primary, Zhou, Feng, primary, and Yang, Dajun, primary

Published
2023
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8. Lisaftoclax in Combination with Alrizomadlin Overcomes Venetoclax Resistance in Acute Myeloid Leukemia and Acute Lymphoblastic Leukemia: Preclinical Studies

Author

Zhai, Yifan, primary, Tang, Qiuqiong, additional, Fang, Douglas D., additional, Deng, Jing, additional, Zhang, Kaixiang, additional, Wang, Qixin, additional, Yin, Yan, additional, Fu, Chengcheng, additional, Xue, Sheng-Li, additional, Li, Na, additional, Zhou, Feng, additional, and Yang, Dajun, additional

Published
2022
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16. Abstract 1096: FMS-like tyrosine kinase 3 (FLT3) inhibition by olverembatinib (HQP1351) downregulates MCL-1 and synergizes with BCL-2 inhibitor APG-2575 in preclinical models of FLT3-mutant acute myeloid leukemia (AML)

Author

Fang, Douglas D., primary, Zhu, Hengrui, additional, Tang, Qiuqiong, additional, Wang, Qixin, additional, Li, Na, additional, Fang, Xu, additional, Min, Ping, additional, Wang, Guangfeng, additional, Yang, Dajun, additional, and Zhai, Yifan, additional

Published
2021
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18. Abstract 4217: Synergy of tyrosine kinase inhibitor HQP1351 and MDM2-P53 antagonist, APG-115, in preclinical models of FLT3 mutant and TP53 wild-type acute myeloid leukemia

Author

Fang, Douglas D., primary, Tang, Qiuqiong, additional, Wang, Qixin, additional, Li, Na, additional, Fang, Xu, additional, Gu, Jiaxing, additional, Kong, Yanhui, additional, Rong, Tao, additional, Wang, Guangfeng, additional, Yang, Dajun, additional, and Zhai, Yifan, additional

Published
2020
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20. Abstract 2058: BCL-2 selective inhibitor APG-2575 synergizes with BTK inhibitor in preclinical xenograft models of follicular lymphoma and diffuse large B-cell lymphoma

Author

Fang, Douglas D., primary, Zhai, Guoqin, additional, Gu, Shoulai, additional, Tao, Ran, additional, Tang, Qiuqiong, additional, Min, Ping, additional, Wang, Qixin, additional, Yang, Dongmei, additional, Gu, Jiaxing, additional, Li, Yinfeng, additional, Chen, Dingxiong, additional, Li, Jiajun, additional, Wang, Guangfeng, additional, Yang, Dajun, additional, and Zhai, Yifan, additional

Published
2019
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23. A plasma metabolite panel as biomarkers for early primary breast cancer detection

Author

Yuan, Baowen, primary, Schafferer, Simon, additional, Tang, Qiuqiong, additional, Scheffler, Matthias, additional, Nees, Juliane, additional, Heil, Jörg, additional, Schott, Sarah, additional, Golatta, Michael, additional, Wallwiener, Markus, additional, Sohn, Christof, additional, Koal, Therese, additional, Wolf, Barbara, additional, Schneeweiß, Andreas, additional, and Burwinkel, Barbara, additional

Published
2019
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24. Evaluation of Promoter Methylation of RASSF1A and ATM in Peripheral Blood of Breast Cancer Patients and Healthy Control Individuals

Author

Cao, Xue, primary, Tang, Qiuqiong, additional, Holland-Letz, Tim, additional, Gündert, Melanie, additional, Cuk, Katarina, additional, Schott, Sarah, additional, Heil, Jörg, additional, Golatta, Michael, additional, Sohn, Christof, additional, Schneeweiss, Andreas, additional, and Burwinkel, Barbara, additional

Published
2018
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29. DNA methylation array analysis identifies breast cancer associated RPTOR, MGRN1 and RAPSN hypomethylation in peripheral blood DNA

Author

Tang, Qiuqiong, primary, Holland-Letz, Tim, additional, Slynko, Alla, additional, Cuk, Katarina, additional, Marme, Frederik, additional, Schott, Sarah, additional, Heil, Jörg, additional, Qu, Bin, additional, Golatta, Michael, additional, Bewerunge-Hudler, Melanie, additional, Sutter, Christian, additional, Surowy, Harald, additional, Wappenschmidt, Barbara, additional, Schmutzler, Rita, additional, Hoth, Markus, additional, Bugert, Peter, additional, Bartram, Claus R., additional, Sohn, Christof, additional, Schneeweiss, Andreas, additional, Yang, Rongxi, additional, and Burwinkel, Barbara, additional

Published
2016
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34. MAP4K4 deletion inhibits proliferation and activation of CD4+ T cell and promotes T regulatory cell generation in vitro.

Author

Huang, Hongpeng, Tang, Qiuqiong, Chu, Hongqian, Jiang, Jianjun, Zhang, Haizhou, Hao, Weidong, and Wei, Xuetao

Subjects
*MITOGEN-activated protein kinases, *DELETION mutation, *CD4 antigen, *T cells, *INHIBITION of cellular proliferation, *IN vitro studies, *INTERLEUKIN-2
Abstract

Highlights: [•] MAP4K4 is required for the proliferation and activation of CD4+ T cells. [•] MAP4K4 deletion in CD4+ T cells suppresses the IL-2 and IFN-γ production. [•] MAP4K4 is essential for promoting the development of CD25+ CD4+ Tregs. [•] MAP4K4 deficiency prevents the phosphorylation of Erk, Jnk, p38 and PKC-θ. [ABSTRACT FROM AUTHOR]

Published
2014
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35. FLT3 inhibition by olverembatinib (HQP1351) downregulates MCL-1 and synergizes with BCL-2 inhibitor lisaftoclax (APG-2575) in preclinical models of FLT3-ITDmutant acute myeloid leukemia

Author

Fang, Douglas D., Zhu, Hengrui, Tang, Qiuqiong, Wang, Guangfeng, Min, Ping, Wang, Qixin, Li, Na, Yang, Dajun, and Zhai, Yifan

Abstract

FLT3-ITDmutations occur in approximately 25% of patients with acute myeloid leukemia (AML) and are associated with poor prognosis. Despite initial efficacy, short duration of response and high relapse rates limit clinical use of selective FLT3 inhibitors. Combination approaches with other targeted therapies may achieve better clinical outcomes.

Published
2022
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36. Blood-based DNA methylation as biomarker for breast cancer: a systematic review

Author

Tang, Qiuqiong, Cheng, Jie, Cao, Xue, Surowy, Harald, and Burwinkel, Barbara

Subjects
610 Medical sciences Medicine
Abstract

Multiple studies have investigated global DNA methylation profiles and gene-specific DNA methylation in blood-based DNA to develop powerful screening markers for cancer. This systematic review summarizes the current evidence on methylation studies that investigated methylation level of blood-derived DNA of breast cancer (BC) patients in comparison to healthy controls by conducting a systematic literature review in PubMed and Web of Science. Essential results, such as methylation levels of BC cases and healthy controls, p values, and odds ratios, were extracted from these studies by two investigators independently. Overall, 45 publications met the inclusion criteria for this review. DNA from whole blood, as well as cell-free DNA (cfDNA) from serum or plasma, was used in these studies. The most common method used for measuring global DNA methylation was the investigation of repetitive elements as surrogates and the application of array-based genome-wide methylation analysis. For measuring gene-specific methylation level, methylation-specific PCR and pyrosequencing were the most frequently used methods. Epigenome-wide blood DNA hypomethylation in BC patients were reported in several studies; however, the evidence is still not conclusive. The most frequently investigated gene in whole blood was BRCA1, which was found more frequently methylated in patients compared to controls. RASSF1A was the most widely investigated gene in cfDNA of serum or plasma, which was also found more frequently methylated in patients compared to controls. Several of the eligible studies reported the associations of global hypomethylation and increased BC risk. Studies investigated associations between gene-specific methylation and BC risk, while got heterogeneous results. But two studies reported that hypermethylation of ATM gene was associated with increased BC risk, which suggest the potential use of this gene for BC risk stratification. Overall, our review suggests the possibility of using blood-based DNA methylation marker as promising marker for BC risk stratification, as several studies found associations between certain methylation level in blood and BC risk. However, so far, the evidence is still quite limited. Optimal markers are yet to be developed and promising results needed to be validated in prospective study cohorts and tested in large screening populations.

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37. Lisaftoclax in Combination with Alrizomadlin Overcomes Venetoclax Resistance in Acute Myeloid Leukemia and Acute Lymphoblastic Leukemia: Preclinical Studies.

Author

Zhai Y, Tang Q, Fang DD, Deng J, Zhang K, Wang Q, Yin Y, Fu C, Xue SL, Li N, Zhou F, and Yang D

Subjects
Humans, Animals, Mice, Proto-Oncogene Proteins c-bcl-2, Cell Line, Tumor, Bridged Bicyclo Compounds, Heterocyclic pharmacology, Bridged Bicyclo Compounds, Heterocyclic therapeutic use, Apoptosis, Leukemia, Myeloid, Acute drug therapy, Leukemia, Myeloid, Acute genetics, Leukemia, Myeloid, Acute pathology, Antineoplastic Agents therapeutic use, Precursor Cell Lymphoblastic Leukemia-Lymphoma drug therapy, Precursor Cell Lymphoblastic Leukemia-Lymphoma genetics
Abstract

Purpose: Despite approval of B-cell lymphoma (BCL)-2 inhibitor venetoclax for certain hematologic malignancies, its broader clinical benefit is curtailed by resistance. Our study aimed to determine if treatment with novel anticancer agents targeting BCL-2 and mouse double minute 2 (MDM2) could overcome venetoclax resistance in preclinical models., Experimental Design: Venetoclax-sensitive and venetoclax-resistant acute myeloid leukemia (AML) and acute lymphoblastic leukemia cells and xenograft models were used to evaluate antitumor effects and underlying mechanisms associated with combined BCL-2 inhibitor lisaftoclax (APG-2575) and MDM2 inhibitor alrizomadlin (APG-115)., Results: The combination exhibited synergistic antiproliferative and apoptogenic activities in TP53 wild-type AML cell lines in vitro. This synergy was further exemplified by deep antitumor responses and prolonged survival in AML cell line-derived and patient-derived xenograft models. Interestingly, the combination treatment resensitized (to apoptosis) venetoclax-resistant cellular and mouse models established via chronic drug exposure or genetically engineered with clinically relevant BCL-2 gene mutations. Synergistic effects in reducing cellular viability and proliferation were also demonstrated in primary samples of patients with venetoclax-resistant AML treated with lisaftoclax and alrizomadlin ex vivo. Mechanistically, alrizomadlin likely primes cancer cells to BCL-2 inhibition-induced cellular apoptosis by downregulating expression of antiapoptotic proteins myeloid cell leukemia-1 and BCL-extra-large and upregulating pro-death BCL-2-associated X protein., Conclusions: Lisaftoclax in combination with alrizomadlin overcomes venetoclax resistance mediated by various mechanisms, including BCL-2 mutations. In addition, we posit further, putative molecular mechanisms. Our data rationalize clinical development of this treatment combination in patients with diseases that are insensitive or resistant to venetoclax., (©2022 American Association for Cancer Research.)

Published
2023
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38. Let-7 g is involved in doxorubicin induced myocardial injury.

Author

Fu J, Peng C, Wang W, Jin H, Tang Q, and Wei X

Subjects
Animals, Blood Pressure, Cell Survival, Cells, Cultured, Disease Models, Animal, Down-Regulation, Heart Diseases chemically induced, Heart Diseases metabolism, Heart Diseases pathology, Heart Diseases physiopathology, Heart Rate, Male, Myocytes, Cardiac pathology, Rats, Rats, Wistar, Real-Time Polymerase Chain Reaction, Reverse Transcriptase Polymerase Chain Reaction, Time Factors, Troponin T blood, Antibiotics, Antineoplastic, Doxorubicin, Heart Diseases genetics, MicroRNAs metabolism, Myocytes, Cardiac metabolism
Abstract

Objectives: To investigate whether let-7 g (miRNA) was involved in doxorubicin-induced cardiotoxicity., Methods: Rats were treated with doxorubicin at increasing doses (0mg/kg, 6 mg/kg, 12 mg/kg, 18 mg/kg). Heart rate, pulse pressure and plasma cardiac troponin T concentrations were measured. Primary cultured myocardial cells were incubated with DOX at increasing concentrations (0 μmol/l, 0.004 μmol/l, 0.02 μmol/l, 0.1 μmol/l, 0.5 μmol/l) for 24h. Cellular viability and the beat frequency were measured. For both rats and cultured cells, miRNA content was measured by real-time reverse-transcription PCR., Results: All DOX-treated rats had a decrease in heart rate, an increase in pulse pressure compared with control group after injections (p<0.05). Concentration of cTnT was increased significantly in 18 mg/kg group. Content of let-7 g decreased significantly (p<0.05) in 18 mg/kg group in vivo and all the doxorubicin treated group in vitro., Conclusions: The down regulation of let-7 g in the myocardial-injury model suggests that let-7 g may play an important role in the development of cardiac disease., (Copyright © 2012. Published by Elsevier B.V.)

Published
2012
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