Academic literature on the topic 'Wang Zhiyuan'

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Journal articles on the topic "Wang Zhiyuan"

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Anshu, Shi, François Lachapelle, and Matthew Galway. "The recasting of Chinese socialism: The Chinese New Left since 2000." China Information 32, no. 1 (March 2018): 139–59. http://dx.doi.org/10.1177/0920203x18760416.

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In post-Mao China, a group of Chinese intellectuals who formed what became the New Left (新左派) sought to renew socialism in China in a context of globalization and the rise of social inequalities they associated with neo-liberalism. As they saw it, China’s market reform and opening to the world had not brought greater equality and prosperity for all Chinese citizens. As part of China Information’s research dialogue on the intellectual public sphere in China, this article provides a historical survey of the development of the contemporary Chinese New Left, exploring the range of ideas that characterized this intellectual movement. It takes as its focus four of the most prominent New Left figures and their positions in the ongoing debate about China’s future: Wang Shaoguang, Cui Zhiyuan, Wang Hui, and Gan Yang.
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Chen, Chia-Chun, Kai Song, Wendy Tran, Matthew Obusan, Tyler Sugimoto, Katherine Sheu, Donghui Cheng, et al. "Abstract 789: Elucidating transcriptional dynamics in neuroendocrine differentiation of advanced prostate cancer." Cancer Research 82, no. 12_Supplement (June 15, 2022): 789. http://dx.doi.org/10.1158/1538-7445.am2022-789.

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Abstract Small cell carcinomas of the lung, bladder, and prostate share similar transcription patterns and drug sensitivities. Due to their high cellular plasticity, these cancers often escape treatment through a trans-differentiation from adenocarcinoma to the neuroendocrine state. We previously developed a pan small cell cancer in vitro/in vivo model named PARCB that can recapitulate this transition from primary patient tissues. To understand which transcription factors may be important in this transition, we conducted bulk and single cell RNA sequencing over time. We identified a developmental trajectory that is shared among all samples and is defined by stage-specific transcription factors. We plan to interrogate the role that these transcription factors play in the PARCB transformation assay. We performed ATAC sequencing to investigate how these transcription factors regulate these transitional states. Our study will provide a basic understanding of the transcriptional changes that occur during neuroendocrine differentiation and provide new potential therapeutic targets for small cell cancers. Citation Format: Chia-Chun Chen, Kai Song, Wendy Tran, Matthew Obusan, Tyler Sugimoto, Katherine Sheu, Donghui Cheng, Grigor Varuzhanyan, Liang Wang, Lisa Ta, Zhiyuan Mao, Nathanael Bangayan, Jung-Wook Park, Thomas Graerber, Owen Witte. Elucidating transcriptional dynamics in neuroendocrine differentiation of advanced prostate cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 789.
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Zhao, Hui, zhiyuan jiang, zhiyu wang, yujie chang, and shunyi ruan. "Abstract 5665: LILRB2 mediates the immune escape of breast tumor cells by degrading HLA-A." Cancer Research 82, no. 12_Supplement (June 15, 2022): 5665. http://dx.doi.org/10.1158/1538-7445.am2022-5665.

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Abstract Breast cancer has now risen to the number one cancer in the world, posing a great threat to human health. LILRB2 (leukocyte immunoglobulinlike receptor B2) is an important immunosuppressive receptor protein, which is mainly expressed in myeloid cells, such as macrophages and dendritic cells. At present, we have found clinically that patients with breast cancer bone and bone marrow metastasis have higher expression of LILRB2. In our research, we used Western blotting, real-time fluorescent quantitative Polymerase Chain Reaction (RT-PCR), flow cytometry, and other experimental methods to explore the expression and function of LILRB2 in breast cancer cells. In our research, we found that LILRB2does increase expression in breast cancer cells, therefore, we want to explore the role of LILRB2 in breast cancer cells. we find that LILRB2 will accelerate the proliferation of tumor cells and increase their migration ability. We tested the related signal pathways and found that LILRB2 can promote the enhancement of the NF-Kb signal pathway. Further, we have done related LILRB2 correlation analysis and found that LILRB2 can reduce human leukocyte antigen-A (HLA-A) Expression. Next, we tested the changes in the level of major histocompatibility complex (MHC-1) related mRNA and found that its mRNA expression increased, which was inconsistent with the decrease in its protein level we observed. Therefore, we used the proteasome inhibitor MG132 for treatment, and the results showed after adding MG132, the decrease in HLA-A expression caused by overexpression of LILRB2 was restored. Next, we knocked down the breast cancer cell line of membrane-associated ring finger (MARCH9). After we knocked down MARCH9, transfection of LILRB2 did not increase the ubiquitination of HLA-A. Therefore we show that LILRB2 can mediate the post-translational modification of HLA-A via MARCH9, which in turn mediates the degradation ofHLA-A. In conclusion, our research shows that LILRB2 maybe a candidate of clinical target for the treatment of breast cancer, preventing possible bone and bone marrow metastasis from breast cancer. Citation Format: Hui Zhao, zhiyuan jiang, zhiyu wang, yujie chang, shunyi ruan. LILRB2 mediates the immune escape of breast tumor cells by degrading HLA-A [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 5665.
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Cao, Zhiyuan, Chengfei Pu, Xianyang Jiang, Guiting Han, Yuzhe Peng, Wensheng Wang, Wei Ding, et al. "Abstract 2838: Antigen-independent expansion enhances efficacy of CAR-T cells against solid tumor." Cancer Research 82, no. 12_Supplement (June 15, 2022): 2838. http://dx.doi.org/10.1158/1538-7445.am2022-2838.

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Abstract One key hurdle for the CAR-T cell treatment of solid tumors is the limited accessibility of solid tumor antigens outside the tumor microenvironment, which prohibits the expansion of solid tumor-targeting CAR-T cells in patients. Here, we report the characterization of prostatic acid phosphatase (PAP) as a feasible CAR-T target for prostate cancer and a novel approach, named CoupledCAR, to expand solid tumor-targeting CAR-T cells lacking solid tumor antigens based on the observation of non-transduced T cells proliferating together with CD19 CAR-T cells during the treatment of acute lymphocyte leukemia. We demonstrated that CoupledCAR can significantly enhance the expansion and antitumor efficacy of PAP CAR-T cells both in vitro and in vivo. Furthermore, we showed that the expansion of solid tumor-targeting CAR-T cells does not depend on CAR/CD3ζ stimulation through direct antigen binding with CAR but enhances the memory status of CAR-T cells and causes little exhaustion. Since the CoupledCAR system does not rely on solid tumor antigens, we propose that it can be utilized in all CAR-T and T cell therapies for the treatment of solid tumors. Citation Format: Zhiyuan Cao, Chengfei Pu, Xianyang Jiang, Guiting Han, Yuzhe Peng, Wensheng Wang, Wei Ding, Xiaogang Shen, Dongqi chen, Beibei Jia, Xiaoqiang Xu, Zhipeng Huang, Xi Huang, Wenbi Liu, Ruihong Zhu, Lee Tian, Christopher Ballas, Victor.X Lu, Zhao Wu, Lei Xiao. Antigen-independent expansion enhances efficacy of CAR-T cells against solid tumor [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 2838.
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Wang, Ruiping, Shumei Song, Jiangjiang Qin, Yuan Li, Yibo Fan, Deyali Chatterjee, Ghia Tatlonghari, et al. "Abstract 5017: A single-cell atlas of tumor microenvironment defines the continuum of gastric adenocarcinoma tumorigenesis and progression." Cancer Research 82, no. 12_Supplement (June 15, 2022): 5017. http://dx.doi.org/10.1158/1538-7445.am2022-5017.

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Abstract Gastric adenocarcinoma (GAC), a global health burden, lacks detail understanding of the evolution-driven cellular/molecular programs that lead to GAC tumorigenesis followed by progression/metastases. The definition of the interplay(s) between immune/stromal cells and premalignant/malignant GAC cells could propel us into a new dimension of understanding and therapeutics. Here, we performed a comprehensive single-cell profiling of 68 specimens collected from 43 subjects including non-neoplastic tumor adjacent tissue, precancerous lesions, localized, and metastatic GACs. We profiled a total of 77,392 high-quality cells which revealed 62 unique cell states uncovering varying profiles. We define alterations in TMEs that underscore initiation of tumorigenesis to eventual progression. For instance, we found a striking preponderance of B lineage cells, primarily the IgA+ plasma cells, in TMEs of the precancerous lesions, whereas 3 immunosuppressive myeloid subsets with high expression of genes signature including SPP1, LAIR1, SIRPA, TIM-3, TGFB1, and MARCO dominated in advanced GACs. We observed that fractions of GZMK+ effector CD8 T cells and progenitor exhausted CD8 T cells gradually increased as GACs progressed to advanced stages with highest abundant in metastatic GACs. In addition, our analysis revealed extensive stromal remodeling along the GAC continuum, which may have contributed to enhanced angiogenesis and progressive immune suppressive signaling. Notably, we uncovered 3 unique TME interactomes that are defined by 6 cellular environtypes that provide context-dependent definition and granularity to GAC networks inhabited by 62 TME cell subsets giving GAC to a novel landscape not yet defined. The two distinct environtypes in GAC primaries are validated in three independent large-scale GAC cohorts, giving credence and definition to previously established histopathological variables, genomic/molecular subtypes and clinical outcomes. The analysis of tumor associated stromal cells discovered SDC2 as an exploitable target to pursue. SDC2 was not only abundant in the stroma, but the abundance is validated in 3 independent single-cell GAC cohorts as well as at the protein level using independent approaches. Overexpression of SDC2 formed a gradient from early GAC to metastatic and is prognostic in large-scale GAC cohorts examined. This study provides an atlas of GAC TMEs from tumorigenesis to advanced GAC that could be further developed for novel therapeutics but also serves as a community resource. Citation Format: Ruiping Wang, Shumei Song, Jiangjiang Qin, Yuan Li, Yibo Fan, Deyali Chatterjee, Ghia Tatlonghari, Zhiyuan Xu, Can Hu, Shaowei Mo, Matheus D. Sewastjanow, Ahmed Adel Fouad Abdelhakeem, Zhenning Wang, Xiangdong Cheng, Jaffer A. Ajani, Linghua Wang. A single-cell atlas of tumor microenvironment defines the continuum of gastric adenocarcinoma tumorigenesis and progression [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 5017.
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Zhao, Hui, Yujie Chang, Zhiyuan Jiang, Zhiyu Wang, and Shunyi Ruan. "Abstract CT543: 18F-FDG PET/CT detects potentially malignant bone metastases in patients with suspected lesions: A prospective clinical trial." Cancer Research 82, no. 12_Supplement (June 15, 2022): CT543. http://dx.doi.org/10.1158/1538-7445.am2022-ct543.

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Abstract Tumor metastasis to the skeleton affects over 70% cancer patients, more than any other site of metastasis Skeletal related events (SREs) included spinal cord compression, fracture, bone radiation or surgery, and tumor-related hypercalcemia are severe complications of bone metastases, which impair patients life quality and require particular treatments The gold standard for the definitive diagnosis is still pathological examination, which needs pre-biopsy imaging review to improve the diagnosis efficacy Classic imaging review method for being CT (Computed Tomography) and 18F-FDG PET/CT Research has shown that 18F-FDG PET/CT is superior to CT in detecting bone metastasis, however, it is not validated by a prospective study Besides, as SUVmax is a metabolic parameter in oncology imaging, we can serve as a reliable semiquantitative indicator to differentiate bone lesions We conducted a prospective clinical trial at Shanghai Sixth People’s Hospital Inclusion criteria were as follows: referred for diagnostic biopsy on a suspicion of metastatic disease Exclusion criteria included contraindications for biopsy 205 patients participated in the cohort study, then were randomized into PET/CT and CT group They underwent 18F-FDG PET/CT and CT separately to confirm accurate location, then both received CT-guided bone biopsy to confirm The sensitivity, specificity and accuracy were calculated In PET/CT group, malignant bone metastases were found in 83/137 patients and biopsies proved 80 were actual metastases In CT group, 48 malignant bone metastases were spotted and 47 were truly decisive The sensitivity, specificity and accuracy of 18F-FDG PET/CT and CT are 99% vs 87%, 95% vs 93%, and 97% vs 88% A chi-square test was utilized to analyze The sensitivity of 18F-FDG PET/CT is better than CT (P=0 0065), but the specificity and accuracy had no differences, indicating 18F-FDG PET/CT could detect more bone metastatic lesions potentially than CT We also found metastasis malignant lesions had higher bone SUVmax than benign (median 9 3 vs 4 25, p <0 001) ROC curves were asked to evaluate the differential efficacy of SUVmax In all 137 patients, the SUVmax 6 3 showed an AUC of 0 874 to predict malignant metastases Our research shows that [18F]FDG PET/CT has greater sensitivity in detecting malignant bone metastases than CT, and SUVmax can be different criteria for determining the malignancy of bone lesions Citation Format: Hui Zhao, Yujie Chang, Zhiyuan Jiang, Zhiyu Wang, Shunyi Ruan. 18F-FDG PET/CT detects potentially malignant bone metastases in patients with suspected lesions: A prospective clinical trial [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr CT543.
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Ta, Lisa H., Janai R. Carr-Ascher, Weixian Deng, Brandon L. Tsai, Wendy Tran, Donny Gun, Donghui Cheng, et al. "Abstract 2438: Determining the role of non-mutated C-Raf kinase in metastatic disease." Cancer Research 82, no. 12_Supplement (June 15, 2022): 2438. http://dx.doi.org/10.1158/1538-7445.am2022-2438.

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Abstract Many aggressive epithelial cancers do not carry targetable driver mutations (Mendiratta et al. 2021, NCI-MATCH Clinical trial NCT02465060). Commonly altered signaling pathways highlight the propensity for tumors to depend on such pathways for growth and survival where genomic alterations may not be required for pathway activation. The Raf family kinases are crucial mediators of the Ras/Raf/MEK/ERK (MAPK) cascade, which has been shown to be upregulated in a subset of metastatic cancers and are mutated in many epithelial cancers. A recent study suggests non-mutated C-Raf can drive metastasis to the lungs, bone, and various other tissues (Faltermeir et al. 2016). Though the mechanism of C-Raf driven metastasis is likely through MAPK activation, C-Raf has been demonstrated to possess MAPK independent roles that may also contribute to this phenotype. In this study, we explored various C-Raf functions as drivers of metastasis in an intracardiac mouse model system. Using a series of Raf knock-out cell lines and mutants targeting functional residues in C-Raf, we demonstrated that C-Raf dimerization is necessary to drive metastasis. We further showed that the metastasis-promoting activity of C-Raf is dependent on co-expression of its family member, B-Raf, for an accelerated metastatic phenotype. However, overexpression of a kinase-dead C-Raf mutant was still able to produce metastases albeit with lower efficiency, suggesting C-Raf possesses non-kinase dependent functions that also contributed to metastasis. Together, these results point to the importance of Raf non-canonical roles in oncogenic processes that may be unappreciated in metastatic disease. Citation Format: Lisa H. Ta, Janai R. Carr-Ascher, Weixian Deng, Brandon L. Tsai, Wendy Tran, Donny Gun, Donghui Cheng, Jihui Sha, Yeonjoo Hwang, John W. Phillips, Matthew B. Obusan, Nathanael J. Bangayan, Miyako Noguchi, Zhiyuan Mao, Chia-Chun Chen, Liang Wang, Grigor Varuzhanyan, John D. Gordon, James W. Wohlschlegel, Owen N. Witte. Determining the role of non-mutated C-Raf kinase in metastatic disease [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 2438.
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Li, Ying-ying, Zhiyuan Peng, Shuaijun Sun, Kun Guo, Deming Kong, Xiaomin Li, Yuning Xie, et al. "Abstract 5486: ENPP1 inhibitor ZX-8177 enhances anti-tumor activity of conventional therapies by modulating tumor microenvironment." Cancer Research 82, no. 12_Supplement (June 15, 2022): 5486. http://dx.doi.org/10.1158/1538-7445.am2022-5486.

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Abstract Emerging studies revealed that tumor derived 2’3’-cGAMP could act as an immune transmitter and directly trigger anti-tumor immunity. Damage associated molecular patterns, e.g. damaged genomic DNA, released from injured cancer cells can be converted into 2’, 3’-cGAMP by cGAS. Subsequently, cGAMP triggers STING pathway activation to produce type I interferons (IFNs) and other related innate immunity in the tumor microenvironment. Ecto-nucleotide pyrophosphatase/phosphodiesterase-1 (ENPP1), a membrane-bound nucleotide hydrolase, has been discovered as the predominant enzyme hydrolyzing 2’3’-cGAMP (Li, et al). Hence, ENPP1 blockade in the tumor milieu is a potential strategy against tumors by improving innate immunity response. In this report, we present a potent ENPP1 inhibitor ZX-8177. ZX-8177 showed an IC50 of 9.5 nM in a biochemical assay and an IC50 of 11 nM in MDA-MB-231 cell-based enzymatic assay. In a functional assay for evaluating efficacy of ZX-8177, the production of IFN-β1 by THP-1 cells was measured after the cells were cultured in the conditioned medium collected from MDA-MB-231 cells treated with or without ZX-8177. The interferon production assay showed an EC50 of 15 pM, suggesting that ZX-8177 effectively facilitated IFN-β1 production via cGAMP-STING axis. In CT-26 syngeneic mouse model, ZX-8177 treatment at 2 mg/kg, BID for 14 days can achieve around 37-60% tumor growth inhibition (TGI). No body weight loss was observed during treatment. Flow cytometry analysis indicated that ZX-8177 treatment resulted in a 2-3-fold increase in tumor-infiltrating NK (CD314+CD335+) cells, cytotoxic CD8 T cells (GranzB+CD8+), and M1-macrophages (CD206-MHCII+); and a decrease in M2-macrophages (CD206+MHCII-) (p< 0.05). Combination of Mitomycin C (0.5 mg/kg, i.p., BIW) and ZX-8177 (2 mg/kg, i.p., BID) in CT-26 model yielded synergistic anti-tumor efficacy (increased >30% TGI). The level of cGAMP in tumor tissue harvested from the combination treatment group was around 2-fold higher than that in the vehicle group. Furthermore, synergistic tumor inhibition of ZX-8177 and anti-PD-L1 antibody was also observed in MC38 mouse model. TGI of anti-PD-L1 antibody vs. combo treatment is 53% vs. 75%, p < 0.05. ZX-8177 has a favorable DMPK and safety pharmacology profile to support it as a clinical candidate for further development. Citation Format: Ying-ying Li, Zhiyuan Peng, Shuaijun Sun, Kun Guo, Deming Kong, Xiaomin Li, Yuning Xie, Siyu Shui, Yin Wang, Jinfu Yang, Xiaolin Alan Hao, Xiaoli (Shelley) Qin. ENPP1 inhibitor ZX-8177 enhances anti-tumor activity of conventional therapies by modulating tumor microenvironment [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 5486.
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Lee, Dean, Monika Manne, Roshan Kumar, Rebecca Silver, Alexandra Staskus, Julianna Crivello, Zhiyuan Wang, et al. "Abstract 618: Discovery of predictive biomarkers of response to T cell-targeting biologics using ex vivo single-cell profiling coupled with TCR clonotype characterization." Cancer Research 82, no. 12_Supplement (June 15, 2022): 618. http://dx.doi.org/10.1158/1538-7445.am2022-618.

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Abstract The discovery of predictive biomarkers of response is critical for forecasting patient benefit from novel immune-modulatory therapeutics. However, their discovery is hindered by the complexity of the drug modes of action and the lack of adequate biological models. We designed an approach to define biomarkers of response by subjecting dissociated tissue from human tumors to T cell-targeting biologics or their combinations, followed by single-cell transcriptomic profiling and TCR clonotype characterization. Responding cells are identified as those showing treatment-specific shifts in gene expression profiles. Specifically for T cells, TCR clonotypes can be used to match responding T cells in treatment conditions to their sister clones in the baseline state. Comparing the baseline gene expression profiles between T cell clonotypes that responded to the treatment and those that did not allows the discovery of gene expression signatures that can predict response. We processed over 20 tumor samples obtained from cancer patients and treated them ex vivo with two novel biologics currently under clinical development - HFB301001, a potentially best-in-class 2nd generation OX40 agonist, and HFB200301, a potentially first-in-class TNFR2 agonist. We applied our biomarker discovery strategy to the pooled scRNA-seq and scTCR-seq data from these samples to define predictive signatures of response to these drugs. To further validate this strategy, we also generated single-cell data in our ex vivo system to characterize response to anti-PD-1 treatment. In the anti-PD-1 predictive response signature, we identified genes involved in inflammatory response and genes in the pathway of other co-inhibitory checkpoints. Application of the anti-PD-1 predictive response signature to bulk transcriptomic data from clinical studies with checkpoint inhibitors successfully stratified patients into two groups with significantly different risk of progression. The predictive response signatures for the two novel agonistic antibodies shared genes involved in inflammatory pathway with the anti-PD-1 signature, but also contained other distinct gene sets. Application of these predictive response signatures to bulk transcriptomic data from TCGA was able to stratify patients across cancer indications by predicted likelihood of response to individual treatments or combinations. The predictive biomarkers of response for the novel OX40 and TNFR2 agonist antibodies will be validated in our Phase I clinical trials. Ex vivo single-cell profiling coupled with TCR clonotype characterization enabled the discovery of predictive response signatures that informed patient selection strategies for the early clinical development of novel therapeutics. Citation Format: Dean Lee, Monika Manne, Roshan Kumar, Rebecca Silver, Alexandra Staskus, Julianna Crivello, Zhiyuan Wang, Dohyun Lee, Ross Fulton, Zhizhan Gu, Christos Hatzis, Francisco Adrian, Andreas Raue, Liang Schweizer. Discovery of predictive biomarkers of response to T cell-targeting biologics using ex vivo single-cell profiling coupled with TCR clonotype characterization [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 618.
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Zhang, Zhenqing, Yunli Jia, Xiaoniu Miao, Weifeng Huang, Chao Wang, Zhijun Yuan, Wenchao Jiang, Zhiyuan Li, Liandi Chen, and Andy Tsun. "Abstract 6115: Development of functionally differentiating anti-CD73 antibodies for cancer therapy." Cancer Research 82, no. 12_Supplement (June 15, 2022): 6115. http://dx.doi.org/10.1158/1538-7445.am2022-6115.

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Abstract Background: Although the discovery and development of first-generation of immune checkpoint inhibitors (towards PD1 and CTLA-4) was a major milestone for cancer therapy, current clinical response rates are still considered very limited. Combination treatments are predicted to improve on these current immunotherapies including the targeting of the adenosine pathway (CD39, CD73 or A2AR), which has shown a lot of promise in preclinical and early clinical studies. CD73 is an ecto-5′-nucleotidase which transforms adenosine monophosphate (AMP) to adenosine. Adenosine is a soluble immunosuppressive metabolite that can suppress natural killer cells and cytotoxic CD8+ T cells. Blockade of CD73-mediated conversion of AMP to adenosine may therefore recover anti-tumor immunity through preventing the enrichment of adenosine in the tumor microenvironment. Method: In this campaign, two humanized and Fc-silenced IgG antibodies were generated named 7002-01 and 7002-04. The target binding epitopes of these candidates were revealed by binning experiments through bio-layer interferometry. Cell binding experiments were tested on human and cynomolgus CD73 overexpression CHO cell lines by flow cytometry. Cellular CD73 enzyme inhibition experiments were tested using A375, MDA-MB-231, H2030 and BT549 tumor cell lines via the CellTiter-Glo method. Soluble CD73 enzymatic tests were carried out on patient sera or recombinant CD73 protein using a similar method. T cell proliferation assays were performed using PBMC. In vivo efficacy studies were tested in B-NDG B2M-KO mice that were injected subcutaneously with A375 tumor cells and human PBMC. Results: Two candidates, 7002-01 and 7002-04, were selected based on their functional activity, that recognize different non-overlapping binding epitopes on CD73. Both candidates selectively bind to and can inhibit the activities of both membrane-bound and soluble human CD73 to high levels and seem to maintain inhibition at high dose-ranges without a hook effect. Both candidates can potently rescue adenosine-mediated T cell regulation. Additionally, 7002-01 and 7002-04 have combination synergy or additive effects for CD73 inhibition on soluble CD73, tumor cell lines that express CD73, and PBMC. 7002-01 and 7002-04 have single-agent anti-tumor efficacy and combination synergy with anti-PD1 antibodies in mice. 7002-01 has a typical antibody-like PK profile when rhesus monkeys were administered with a single intravenous dose at 25 or 50 mg/kg. No drug-related toxicities have been observed in GLP toxicity studies with dosages at 50, 250, and 500 mg/kg (QW, 4 weeks). Conclusion: Highly differentiating anti-CD73 antibodies were discovered that show maximal inhibition of both membranous and soluble CD73 without hook effects at high concentrations. 7002-01 was chosen as the lead molecule for its better overall activity profile and should be entering clinical trials by early 2022. Citation Format: Zhenqing Zhang, Yunli Jia, Xiaoniu Miao, Weifeng Huang, Chao Wang, Zhijun Yuan, Wenchao Jiang, Zhiyuan Li, Liandi Chen, Andy Tsun. Development of functionally differentiating anti-CD73 antibodies for cancer therapy [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 6115.
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Dissertations / Theses on the topic "Wang Zhiyuan"

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Wang, Zhiyuan Verfasser], Rüdiger-A. [Akademischer Betreuer] [Eichel, and Marcel [Akademischer Betreuer] Liauw. "Oxygen reduction reaction and oxygen evolution reaction mechanisms investigation of the non-noble bifunctional electrocatalysts in alkaline electrolyte / Zhiyuan Wang ; Rüdiger-Albert Eichel, Marcel Liauw." Aachen : Universitätsbibliothek der RWTH Aachen, 2018. http://d-nb.info/1169915191/34.

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Wang, Zhiyuan [Verfasser], Rüdiger-A. [Akademischer Betreuer] Eichel, and Marcel [Akademischer Betreuer] Liauw. "Oxygen reduction reaction and oxygen evolution reaction mechanisms investigation of the non-noble bifunctional electrocatalysts in alkaline electrolyte / Zhiyuan Wang ; Rüdiger-Albert Eichel, Marcel Liauw." Aachen : Universitätsbibliothek der RWTH Aachen, 2018. http://d-nb.info/1169915191/34.

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(9874106), AJ Ash. "A local analysis of contemporary Chinese/- Australian art by Guan Wei, Wang Zhiyuan and Ah Xian using a global aesthetic." Thesis, 2005. https://figshare.com/articles/thesis/A_local_analysis_of_contemporary_Chinese_-_Australian_art_by_Guan_Wei_Wang_Zhiyuan_and_Ah_Xian_using_a_global_aesthetic/13422644.

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Study examines "the contemporary art practice of three diasporic artists: Guan Wei, Wang Zhiyuan, and Ah Xian and documents their practice and analyses their work using contextual methods".. This project sheds light on Australian art that reflects an emerging global aesthetic. I map the historically oriented relations of artistic exchange in the Asia-Australia region with a focus on contemporary hybrid art created by diasporic artists. I am primarily concerned with the mobile and adaptive cultural exchanges between cultures in response to globalisation. Globalisation is seen as the tension between the global and the local where each informs the other. The underlying processes of globalisation are used to develop an aesthetic that underpins contemporary hybrid art practice located on the interstice between the global and local. I outline a new aesthetics to engage with such transformational art based on multiaxiality, dispersion, transience, unassimilabilty, translation and hybridity. Through case study, I address the contemporary art practice of three diasporic artists: Guan Wei, Wang Zhiyuan, and Ah Xian using a global aesthetic. Taking the artwork of these artists, I document their practice and analyse their work using contextual methods. Finally, I detail the outcomes and syntheses of the research emerging from history, place, theory and most importantly art practice informed by globalisation. The study has implications for artists, theorists, historians, and critics concerning specifically Chinese/-Australian art and contemporary hybrid art in Australia and Asia.

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Books on the topic "Wang Zhiyuan"

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Zang li: Wang Zhiyuan shi ji. Taoyuan Shi: Dou dian wen chuang jie she, 2011.

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Wang Zhen yu Tao Zhiyue. Beijing Shi: Hua wen chu ban she, 2001.

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Wang Zhiyuan: Bigger, Better, and Cheaper. Skira Editore, 2017.

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Chen, Zhuangying, and Achim Aurnhammer, eds. Deutsch-chinesische Helden und Anti-Helden. Ergon Verlag, 2020. http://dx.doi.org/10.5771/9783956506093.

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This volume elucidates the changing relationship between heroization and othering in a German-Chinese cultural comparison. Intercultural case studies illustrate which representatives of German culture and history were subjected to a process of heroization or were disparaged as negative anti-heroes in Chinese culture. Vice versa, Chinese figures who adopted a corresponding heroic or antiheroic function within the German-speaking world are also examined. This German-Chinese dialogue, in which cultural scientists from Germany and China participate, is guided by the assumption that processes of heroization and de-heroization represent paradigmatic focal points in the economics of intercultural transfer. The relationship between individual and collective heroism and the meaning of alienness - be it of Chinese or German characteristics - when importing heroes offer new perspectives insofar as these importations prove to be complex and inconsistent. With contributions by Achim Aurnhammer, Chen Zhuangying, Cong Tingting, Fan Jieping, Olmo Gölz, Joachim Grage, He Zhiyuan, Huang Liaoyu, Hu Chunchun, Hu Kai, Sara Kathrin Landa, Stefanie Lethbridge, Lin Chunjie, Dieter Martin, Isabell Oberle, Dominik Pietzcker, Nicola Spakowski, Jennifer Stapornwongkul, Wang Zhiqiang, Wei Yuquing, Xie Juan, Zhang Fan, Zhu Jianhua, Ulrike Zimmermann.
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Book chapters on the topic "Wang Zhiyuan"

1

Kubin, Wolfgang. "Wang Shizhen: Yiyuan zhiyan." In Kindlers Literatur Lexikon (KLL), 1–2. Stuttgart: J.B. Metzler, 2020. http://dx.doi.org/10.1007/978-3-476-05728-0_21966-1.

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