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2,609 results on '"Hung, Mien–Chie"'

1. Modulation of tumor inflammatory signaling and drug sensitivity by CMTM4

Author

Xu, Yitian, Kang, Kyeongah, Coakley, Brian A, Eisenstein, Samuel, Parveen, Arshiya, Mai, Sunny, Wang, Yuan Shuo, Zheng, Junjun, Boral, Debasish, Mai, Junhua, Pan, William, Zhang, Licheng, Aaronson, Stuart A, Fang, Bingliang, Divino, Celia, Zhang, Bin, Song, Won-Min, Hung, Mien-Chie, Pan, Ping-Ying, and Chen, Shu-Hsia

Published
2025
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3. Astrocyte-induced Cdk5 expedites breast cancer brain metastasis by suppressing MHC-I expression to evade immune recognition

Author

Yuzhalin, Arseniy E., Lowery, Frank J., Saito, Yohei, Yuan, Xiangliang, Yao, Jun, Duan, Yimin, Ding, Jingzhen, Acharya, Sunil, Zhang, Chenyu, Fajardo, Abigail, Chen, Hao-Nien, Wei, Yongkun, Sun, Yutong, Zhang, Lin, Xiao, Yi, Li, Ping, Lorenzi, Philip L., Huse, Jason T., Fan, Huihui, Zhao, Zhongming, Hung, Mien-Chie, and Yu, Dihua

Published
2024
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4. Targeting a chemo-induced adaptive signaling circuit confers therapeutic vulnerabilities in pancreatic cancer

Author

Saito, Yohei, Xiao, Yi, Yao, Jun, Li, Yunhai, Liu, Wendao, Yuzhalin, Arseniy E., Shyu, Yueh-Ming, Li, Hongzhong, Yuan, Xiangliang, Li, Ping, Zhang, Qingling, Li, Ziyi, Wei, Yongkun, Yin, Xuedong, Zhao, Jun, Kariminia, Seyed M., Wu, Yao-Chung, Wang, Jinyang, Yang, Jun, Xia, Weiya, Sun, Yutong, Jho, Eek-hoon, Chiao, Paul J., Hwang, Rosa F., Ying, Haoqiang, Wang, Huamin, Zhao, Zhongming, Maitra, Anirban, Hung, Mien-Chie, DePinho, Ronald A., and Yu, Dihua

Published
2024
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6. Nardilysin-regulated scission mechanism activates polo-like kinase 3 to suppress the development of pancreatic cancer

Author

Fu, Jie, Ling, Jianhua, Li, Ching-Fei, Tsai, Chi-Lin, Yin, Wenjuan, Hou, Junwei, Chen, Ping, Cao, Yu, Kang, Ya’an, Sun, Yichen, Xia, Xianghou, Jiang, Zhou, Furukawa, Kenei, Lu, Yu, Wu, Min, Huang, Qian, Yao, Jun, Hawke, David H., Pan, Bih-Fang, Zhao, Jun, Huang, Jiaxing, Wang, Huamin, Bahassi, E. I. Mustapha, Stambrook, Peter J., Huang, Peng, Fleming, Jason B., Maitra, Anirban, Tainer, John A., Hung, Mien-Chie, Lin, Chunru, and Chiao, Paul J.

Published
2024
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11. Nuclear PD-L1 compartmentalization suppresses tumorigenesis and overcomes immunocheckpoint therapy resistance in mice via histone macroH2A1

Author

Liu, Yong, Yang, Zhi, Wang, Shuanglian, Miao, Rui, Chang, Chiung-Wen Mary, Zhang, Jingyu, Zhang, Xin, Hung, Mien-Chie, and Hou, Junwei

Subjects
Testing, Care and treatment, Models, Dosage and administration, Drug resistance -- Care and treatment -- Models, Immune checkpoint inhibitors -- Dosage and administration -- Testing
Abstract

Introduction Cancer cells can evade attacks from cytotoxic lymphocytes through the interaction of programmed death ligand 1 (PD-L1) with its receptor, programmed cell death protein 1 (PD-1), on the cell [...], Canonically PD-L1 functions as the inhibitory immune checkpoint on cell surface. Recent studies have observed PD-L1 expression in the nucleus of cancer cells. But the biological function of nuclear PD-L1 (nPD-L1) in tumor growth and antitumor immunity is unclear. Here we enforced nPD-L1 expression and established stable cells. nPD-L1 suppressed tumorigenesis and aggressiveness in vitro and in vivo. Compared with PD-L1 deletion, nPD-L1 expression repressed tumor growth and improved survival more markedly in immunocompetent mice. Phosphorylated AMPK[alpha] (p-AMPK[alpha]) facilitated nuclear PD-L1 compartmentalization and then cooperated with it to directly phosphorylate S146 of histone variant macroH2A1 (mH2A1) to epigenetically activate expression of genes of cellular senescence, JAK/STAT, and Hippo signaling pathways. Lipoic acid (LA) that induced nuclear PD-L1 translocation suppressed tumorigenesis and boosted antitumor immunity. Importantly, LA treatment synergized with PD-1 antibody and overcame immune checkpoint blockade (ICB) resistance, which likely resulted from nPD-L1-increased MHC-I expression and sensitivity of tumor cells to interferon-/. These findings offer a conceptual advance for PD-L1 function and suggest LA as a promising therapeutic option for overcoming ICB resistance.

Published
2024
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13. Hormonal therapies up-regulate MANF and overcome female susceptibility to immune checkpoint inhibitor myocarditis

Author

Zhang, Yaohua, Sun, Chengcao, Li, Yajuan, Qin, Juan, Amancherla, Kaushik, Jing, Ying, Hu, Qingsong, Liang, Ke, Zhang, Zhao, Ye, Youqiong, Huang, Lisa A, Nguyen, Tina K, Egranov, Sergey D, Zhao, Zilong, Wu, Andrew, Xi, Yutao, Yao, Jun, Hung, Mien-Chie, Calin, George A, Cheng, Jie, Lim, Bora, Lehmann, Lorenz H, Salem, Joe-Elie, Johnson, Douglas B, Curran, Michael A, Yu, Dihua, Han, Leng, Darabi, Radbod, Yang, Liuqing, Moslehi, Javid J, and Lin, Chunru

Subjects
Cardiovascular, Estrogen, Heart Disease, 5.1 Pharmaceuticals, Aetiology, 2.1 Biological and endogenous factors, Development of treatments and therapeutic interventions, Humans, Female, Male, Mice, Animals, Myocarditis, Immune Checkpoint Inhibitors, Estrogen Receptor beta, Myocytes, Cardiac, Estradiol, Nerve Growth Factors, Biological Sciences, Medical and Health Sciences
Abstract

Immune checkpoint inhibitors (ICIs) have been increasingly used in combination for cancer treatment but are associated with myocarditis. Here, we report that tumor-bearing mice exhibited response to treatment with combinatorial anti-programmed cell death 1 and anti-cytotoxic T lymphocyte antigen-4 antibodies but also presented with cardiovascular toxicities observed clinically with ICI therapy, including myocarditis and arrhythmia. Female mice were preferentially affected with myocarditis compared to male mice, consistent with a previously described genetic model of ICI myocarditis and emerging clinical data. Mechanistically, myocardial tissue from ICI-treated mice, the genetic mouse model, and human heart tissue from affected patients with ICI myocarditis all exhibited down-regulation of MANF (mesencephalic astrocyte-derived neurotrophic factor) and HSPA5 (heat shock 70-kDa protein 5) in the heart; this down-regulation was particularly notable in female mice. ICI myocarditis was amplified by heart-specific genetic deletion of mouse Manf and was attenuated by administration of recombinant MANF protein, suggesting a causal role. Ironically, both MANF and HSPA5 were transcriptionally induced by liganded estrogen receptor β and inhibited by androgen receptor. However, ICI treatment reduced serum estradiol concentration to a greater extent in female compared to male mice. Treatment with an estrogen receptor β-specific agonist and androgen depletion therapy attenuated ICI-associated cardiac effects. Together, our data suggest that ICI treatment inhibits estradiol-dependent expression of MANF/HSPA5 in the heart, curtailing the cardiomyocyte response to immune injury. This endocrine-cardiac-immune pathway offers new insights into the mechanisms of sex differences in cardiac disease and may offer treatment strategies for ICI myocarditis.

Published
2022

25. Rewired m6A epitranscriptomic networks link mutant p53 to neoplastic transformation

Author

Xu, An, Liu, Mo, Huang, Mo-Fan, Zhang, Yang, Hu, Ruifeng, Gingold, Julian A., Liu, Ying, Zhu, Dandan, Chien, Chian-Shiu, Wang, Wei-Chen, Liao, Zian, Yuan, Fei, Hsu, Chih-Wei, Tu, Jian, Yu, Yao, Rosen, Taylor, Xiong, Feng, Jia, Peilin, Yang, Yi-Ping, Bazer, Danielle A., Chen, Ya-Wen, Li, Wenbo, Huff, Chad D., Zhu, Jay-Jiguang, Aguilo, Francesca, Chiou, Shih-Hwa, Boles, Nathan C., Lai, Chien-Chen, Hung, Mien-Chie, Zhao, Zhongming, Van Nostrand, Eric L., Zhao, Ruiying, and Lee, Dung-Fang

Published
2023
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26. PD-L1-mediated gasdermin C expression switches apoptosis to pyroptosis in cancer cells and facilitates tumour necrosis.

Author

Hou, Junwei, Zhao, Rongce, Xia, Weiya, Chang, Chiung-Wen, You, Yun, Hsu, Jung-Mao, Nie, Lei, Chen, Yeh, Wang, Yu-Chuan, Liu, Chunxiao, Wang, Wei-Jan, Wu, Yun, Ke, Baozhen, Hsu, Jennifer, Huang, Kebin, Ye, Zu, Yang, Yi, Xia, Xianghou, Li, Yintao, Li, Chia-Wei, Shao, Bin, Tainer, John, and Hung, Mien-Chie

Subjects
Animals, Apoptosis, B7-H1 Antigen, Biomarkers, Tumor, Cell Proliferation, DNA-Binding Proteins, Female, Gene Expression Regulation, Neoplastic, Humans, Hypoxia, Inflammasomes, Mice, Mice, Inbred BALB C, Mice, Nude, Necrosis, Neoplasms, Pyroptosis, Tumor Cells, Cultured, Tumor-Associated Macrophages, Xenograft Model Antitumor Assays
Abstract

Although pyroptosis is critical for macrophages against pathogen infection, its role and mechanism in cancer cells remains unclear. PD-L1 has been detected in the nucleus, with unknown function. Here we show that PD-L1 switches TNFα-induced apoptosis to pyroptosis in cancer cells, resulting in tumour necrosis. Under hypoxia, p-Stat3 physically interacts with PD-L1 and facilitates its nuclear translocation, enhancing the transcription of the gasdermin C (GSDMC) gene. GSDMC is specifically cleaved by caspase-8 with TNFα treatment, generating a GSDMC N-terminal domain that forms pores on the cell membrane and induces pyroptosis. Nuclear PD-L1, caspase-8 and GSDMC are required for macrophage-derived TNFα-induced tumour necrosis in vivo. Moreover, high expression of GSDMC correlates with poor survival. Antibiotic chemotherapy drugs induce pyroptosis in breast cancer. These findings identify a non-immune checkpoint function of PD-L1 and provide an unexpected concept that GSDMC/caspase-8 mediates a non-canonical pyroptosis pathway in cancer cells, causing tumour necrosis.

Published
2020

27. Hereditary retinoblastoma iPSC model reveals aberrant spliceosome function driving bone malignancies

Author

Tu, Jian, Huo, Zijun, Yu, Yao, Zhu, Dandan, Xu, An, Huang, Mo-Fan, Hu, Ruifeng, Wang, Ruoyu, Gingold, Julian A., Chen, Yi-Hung, Tsai, Kuang-Lei, Forcioli-Conti, Nicolas R., Huang, Sarah X. L., Webb, Thomas R., Su, Jie, Bazer, Danielle A., Ji, Peilin, Yustein, Jason T., Wang, Lisa L., Hung, Mien-Chie, Zhao, Zhongming, Huff, Chad D., Shen, Jingnan, Zhao, Ruiying, and Lee, Dung-Fang

Published
2022

28. Molecular mechanisms of snoRNA-IL-15 crosstalk in adipocyte lipolysis and NK cell rejuvenation

Author

Zhang, Yaohua, Zhao, Zilong, Huang, Lisa A., Liu, Yuan, Yao, Jun, Sun, Chengcao, Li, Yajuan, Zhang, Zhao, Ye, Youqiong, Yuan, Fei, Nguyen, Tina K., Garlapati, Nikhil Reddy, Wu, Andrew, Egranov, Sergey D., Caudle, Abigail S., Sahin, Aysegul A., Lim, Bora, Beretta, Laura, Calin, George A., Yu, Dihua, Hung, Mien-Chie, Curran, Michael A., Rezvani, Katayoun, Gan, Boyi, Tan, Zhi, Han, Leng, Lin, Chunru, and Yang, Liuqing

Published
2023
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31. Osteoprogenitor-GMP crosstalk underpins solid tumor-induced systemic immunosuppression and persists after tumor removal

Author

Hao, Xiaoxin, Shen, Yichao, Chen, Nan, Zhang, Weijie, Valverde, Elizabeth, Wu, Ling, Chan, Hilda L., Xu, Zhan, Yu, Liqun, Gao, Yang, Bado, Igor, Michie, Laura Natalee, Rivas, Charlotte Helena, Dominguez, Luis Becerra, Aguirre, Sergio, Pingel, Bradley C., Wu, Yi-Hsuan, Liu, Fengshuo, Ding, Yunfeng, Edwards, David G., Liu, Jun, Alexander, Angela, Ueno, Naoto T., Hsueh, Po-Ren, Tu, Chih-Yen, Liu, Liang-Chih, Chen, Shu-Hsia, Hung, Mien-Chie, Lim, Bora, and Zhang, Xiang H.-F.

Published
2023
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32. Gasdermin C sensitizes tumor cells to PARP inhibitor therapy in cancer models

Author

Wang, Shuanglian, Chang, Chiung-Wen, Huang, Juan, Zeng, Shan, Zhang, Xin, Hung, Mien-Chie, and Hou, Junwei

Subjects
Care and treatment, Development and progression, Genetic aspects, Dosage and administration, Health aspects, Polymerization inhibitors -- Dosage and administration, Apoptosis -- Health aspects, Cancer -- Development and progression -- Care and treatment -- Genetic aspects, Gene mutation -- Health aspects, Gene mutations -- Health aspects
Abstract

Introduction Poly (ADP-ribose) polymerase inhibitors (PARPi) have been emerging as promising therapeutics for many diseases, including cancer (1). Niraparib, rucaparib, and olaparib have been approved for treatment of patients with [...], Several poly (ADP-ribose) polymerase (PARP) inhibitors (PARPi) are approved by FDA to treat cancer with BRCA mutations. BRCA mutations are considered to fuel a PARPi killing effect by inducing apoptosis. However, resistance to PARPi is frequently observed in the clinic due to an incomplete understanding on the molecular basis of PARPi function and a lack of good markers, beyond BRCA mutations, to predict response. Here, we show that gasdermin C (GSDMC) sensitized tumor cells to PARPi in vitro and in immunocompetent mice and caused durable tumor regression in an immune-dependent manner. A high expression level of GSDMC predicted better response to PARPi treatment in patients with triple-negative breast cancer (TNBC). PARPi treatment triggered GSDMC/caspase-8-mediated cancer cell pyroptosis (CCP) that enhanced PARPi killing of tumor cells. GSDMC-mediated CCP increased memory [CD8.sup.+] T cell population in lymph node (LN), spleen, and tumor and, thus, promoted cytotoxic [CD8.sup.+] T cell infiltration in the tumor microenvironment. T cell-derived granzyme B (GZMB) activated caspase-6, which subsequently cleaved GSDMC to induce pyroptosis. Interestingly, IFN-[gamma] induced GSDMC expression, which, in turn, enhanced the cytotoxicity of PARPi and T cells. Importantly, GSDMC promoted tumor clearance independent of BRCA deficiency in multiple cancer types with PARPi treatment. This study identifies a general marker and target for PARPi therapy and offers insights into the mechanism of PARPi function.

Published
2024
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34. Targeting the ALK–CDK9-Tyr19 kinase cascade sensitizes ovarian and breast tumors to PARP inhibition via destabilization of the P-TEFb complex

Author

Chu, Yu-Yi, Chen, Mei-Kuang, Wei, Yongkun, Lee, Heng-Huan, Xia, Weiya, Wang, Ying-Nai, Yam, Clinton, Hsu, Jennifer L., Wang, Hung-Ling, Chang, Wei-Chao, Yamaguchi, Hirohito, Jiang, Zhou, Liu, Chunxiao, Li, Ching-Fei, Nie, Lei, Chan, Li-Chuan, Gao, Yuan, Wang, Shao-Chun, Liu, Jinsong, Westin, Shannon N., Lee, Sanghoon, Sood, Anil K., Yang, Liuqing, Hortobagyi, Gabriel N., Yu, Dihua, and Hung, Mien-Chie

Published
2022
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40. Histamine N-methyltransferase (HNMT) as a potential auxiliary biomarker for predicting adaptability to anti-HER2 drug treatment in breast cancer patients.

Author

Cheng, Tzu-Chun, Hung, Mien-Chie, Wang, Lu-Hai, Tu, Shih-Hsin, Wu, Chih-Hsiung, Yen, Yun, Chen, Chi-Long, Whang-Peng, Jacqueline, Lee, Wen-Jui, Liao, You-Cheng, Lee, Yu-Ching, Pan, Min-Hsiung, Lin, Hui-Kuan, Tzeng, Huey-En, Guo, Peixuan, Chu, Cheng-Ying, Chen, Li-Ching, and Ho, Yuan-Soon

Subjects
FLUORESCENCE resonance energy transfer, TRIPLE-negative breast cancer, METASTATIC breast cancer, HER2 protein, MEDICAL sciences
Abstract

Background: Up to 23% of breast cancer patients recurred within a decade after trastuzumab treatment. Conversely, one trial found that patients with low HER2 expression and metastatic breast cancer had a positive response to trastuzumab-deruxtecan (T-Dxd). This indicates that relying solely on HER2 as a single diagnostic marker to predict the efficacy of anti-HER2 drugs is insufficient. This study highlights the interaction between histamine N-methyltransferase (HNMT) and HER2 as an adjunct predictor for trastuzumab response. Furthermore, modulation of HER2 expression by HNMT may explain why those with low HER2 expression still respond to T-Dxd. Methods: We investigated the impact of HNMT protein expression on the efficacy of anti-HER2 therapy in both in vivo and ex vivo models of patient-derived xenografts and cell line-derived xenografts. Our analysis included Förster resonance energy transfer (FRET) to assess the interaction strength between HNMT and HER2 proteins in trastuzumab-resistant and sensitive tumor tissues. Additionally, we used fluorescence lifetime imaging microscopy (FLIM), cleaved luciferase, and immunoprecipitation to study the interaction dynamics of HNMT and HER2. Furthermore, we evaluated the influence of HNMT activity on the binding of anti-HER2 antibodies to their targets through flow cytometry. We also observed the nuclear translocation of HNMT/HER2-ICD cells using fluorescent double staining and DeltaVision microscopy. Finally, ChIP sequencing was employed to identify target genes affected by the HNMT/HER2-ICD complex. Results: This study highlights HNMT as a potential auxiliary biomarker for diagnosing HER2 + breast cancer. FRET analysis demonstrated a significant interaction between HNMT and HER2 protein in trastuzumab-sensitive tumor tissue (n = 50), suggesting the potential of HNMT as a predictor of treatment response. Mechanistic studies revealed that the interaction between HNMT and HER2 contributes to increased HER2 protein expression at the transcriptional level, thereby impacting the efficacy of anti-HER2 therapy. Furthermore, a subset of triple-negative breast cancers characterized by HNMT overexpression was found to be sensitive to HER2 antibody–drug conjugates such as T-Dxd. Conclusions: These findings offer crucial insights for clinicians evaluating candidates for anti-HER2 therapy, especially for HER2-low breast cancer patients who could gain from T-Dxd treatment. Identifying HNMT expression could help clinicians pinpoint patients who would benefit from anti-HER2 therapy. [ABSTRACT FROM AUTHOR]

Published
2025
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41. D-ribose-5-phosphate inactivates YAP and functions as a metabolic checkpoint.

Author

Tu, Cheng-E, Liu, Yong-Feng, Liu, Hong-Wei, Jiao, Chun-Mei, Liu, Quentin, Hung, Mien-Chie, Li, Peng, Wan, Xiang-Bo, Fan, Xin-Juan, and Wang, Yun-Long

Subjects
PENTOSE phosphate pathway, YAP signaling proteins, LIFE sciences, CYTOLOGY, MEDICAL sciences
Abstract

Background: Targeting glucose uptake by glucose transporter (GLUT) inhibitors is a therapeutic opportunity, but efforts on GLUT inhibitors have not been successful in the clinic and the underlying mechanism remains unclear. We aim to identify the key metabolic changes responsible for cancer cell survival from glucose limitation and elucidate its mechanism. Methods: The level of phosphorylated YAP was analyzed with Western blotting and Phos-tag immunoblotting. Glucose limitation-induced metabolic changes were analyzed using targeted metabolomics (600MRM). The anti-cancer role of metabolite was examined using colony formation assay and APCmin/+ mice. Co-immunoprecipitation, LS-MS, qRT-PCR, and immunofluorescence were performed to explore the underlying mechanisms. Results: We found that D-Ribose-5-phosphate (D5P), a product of the pentose phosphate pathway connecting glucose metabolism and nucleotide metabolism, functions as a metabolic checkpoint to activate YAP under glucose limitation to promote cancer cell survival. Mechanistically, in glucose-deprived cancer cells, D5P is decreased, which facilitates the interaction between MYH9 and LATS1, resulting in MYH9-mediated LATS1 aggregation, degradation, and further YAP activation. Interestingly, activated YAP further promotes purine nucleoside phosphorylase (PNP)-mediated breakdown of purine nucleoside to restore D5P in a feedback manner. Importantly, D5P synergistically enhances the tumor-suppressive effect of GLUT inhibitors and inhibits cancer progression in mice. Conclusions: Our study identifies D5P as a metabolic checkpoint linking glucose limitation stress and YAP activation, indicating that D5P may be a potential anti-cancer metabolite by enhancing glucose limitation sensitivity. [ABSTRACT FROM AUTHOR]

Published
2025
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42. Ephrin receptor A10 monoclonal antibodies and the derived chimeric antigen receptor T cells exert an antitumor response in mouse models of triple-negative breast cancer

Author

Cha, Jong-Ho, Chan, Li-Chuan, Wang, Ying-Nai, Chu, Yu-Yi, Wang, Chie-Hong, Lee, Heng-Huan, Xia, Weiya, Shyu, Woei-Cherng, Liu, Shih-Ping, Yao, Jun, Chang, Chiung-Wen, Cheng, Fan-Ru, Liu, Jielin, Lim, Seung-Oe, Hsu, Jennifer L., Yang, Wen-Hao, Hortobagyi, Gabriel N., Lin, Chunru, Yang, Liuqing, Yu, Dihua, Jeng, Long-Bin, and Hung, Mien-Chie

Published
2022
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45. Tafenoquine and its derivatives as inhibitors for the severe acute respiratory syndrome coronavirus 2

Author

Chen, Yeh, Yang, Wen-Hao, Chen, Hsiao-Fan, Huang, Li-Min, Gao, Jing-Yan, Lin, Cheng-Wen, Wang, Yu-Chuan, Yang, Chia-Shin, Liu, Yi-Liang, Hou, Mei-Hui, Tsai, Chia-Ling, Chou, Yi-Zhen, Huang, Bao-Yue, Hung, Chian-Fang, Hung, Yu-Lin, Wang, Wei-Jan, Su, Wen-Chi, Kumar, Vathan, Wu, Yu-Chieh, Chao, Shih-Wei, Chang, Chih-Shiang, Chen, Jin-Shing, Chiang, Yu-Ping, Cho, Der-Yang, Jeng, Long-Bin, Tsai, Chang-Hai, and Hung, Mien-Chie

Published
2022
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47. Development and validation of a radiopathomics model to predict pathological complete response to neoadjuvant chemoradiotherapy in locally advanced rectal cancer: a multicentre observational study

Author

Feng, Lili, Liu, Zhenyu, Li, Chaofeng, Li, Zhenhui, Lou, Xiaoying, Shao, Lizhi, Wang, Yunlong, Huang, Yan, Chen, Haiyang, Pang, Xiaolin, Liu, Shuai, He, Fang, Zheng, Jian, Meng, Xiaochun, Xie, Peiyi, Yang, Guanyu, Ding, Yi, Wei, Mingbiao, Yun, Jingping, Hung, Mien-Chie, Zhou, Weihua, Wahl, Daniel R, Lan, Ping, Tian, Jie, and Wan, Xiangbo

Published
2022
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