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Your search keyword '"Shiah, H-S."' showing total 25 results
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25 results on '"Shiah, H-S."'

1. 126P AdvanTIG-105: Phase Ib dose-expansion study of ociperlimab (OCI) + tislelizumab (TIS) in patients (pts) with checkpoint inhibitor (CPI)-experienced advanced non-small cell lung cancer (NSCLC)

Author

Frentzas, S., primary, Meniawy, T., additional, Kao, S.C-H., additional, Coward, J., additional, Clay, T.D., additional, Singhal, N., additional, Black, A., additional, Xu, W., additional, Kumar, R., additional, Lee, Y., additional, Lee, G-W., additional, Liao, W., additional, Zhong, D., additional, Shiah, H-S., additional, Chen, Y-M., additional, Gao, R., additional, Wang, R., additional, Zheng, H., additional, Tan, W., additional, and Cho, E.K., additional

Published
2022
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2. 1017P AdvanTIG-105: Phase Ib dose-expansion study of ociperlimab (OCI) + tislelizumab (TIS) with chemotherapy (chemo) in patients (pts) with metastatic squamous (sq) and non-squamous (non-sq) non-small cell lung cancer (NSCLC)

Author

Yu, Y., primary, Huang, D., additional, Gao, B., additional, Zhao, J., additional, Hu, Y., additional, Zhuang, W., additional, Kao, S., additional, Xu, W., additional, Yao, Y., additional, Yang, T-Y., additional, Lee, Y., additional, Kim, J-S., additional, Shiah, H-S., additional, Wang, R., additional, Zheng, H., additional, Tan, W., additional, Gao, R., additional, Kim, H.R., additional, and Lu, S., additional

Published
2022
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4. 1208P Final results of APOLLO study: Overall survival (OS) of aumolertinib in patients with pretreated EGFR T790M-positive locally advanced or metastatic non-small cell lung cancer (NSCLC)

Author

Lu, S., primary, Wang, Q., additional, Zhang, G., additional, Dong, X., additional, Yang, C-T., additional, Song, Y., additional, Chang, G-C., additional, Lu, Y., additional, Pan, H., additional, Chiu, C-H., additional, Wang, Z., additional, Feng, J., additional, Zhou, J., additional, Xu, X., additional, Guo, R., additional, Chen, J., additional, Yang, H., additional, Chen, Y., additional, Yu, Z., additional, and Shiah, H-S., additional

Published
2021
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6. A KRAS mutation status-stratified randomized phase II trial of gemcitabine and oxaliplatin alone or in combination with cetuximab in advanced biliary tract cancer

Author

Chen, J. S., Hsu, C., Chiang, N. J., Tsai, C. S., Tsou, H. H., Huang, S. F., Bai, L. Y., Chang, I. C., Shiah, H. S., Ho, C. L., Yen, C. J., Lee, K. D., Chiu, C. F., Rau, K. M., Yu, M. S., Yang, Y., Hsieh, R. K., Chang, J. Y., Shan, Y. S., Chao, Y., Chen, L. T., Shen, Wen-Chi, Hsu, Hung-Chih, Hsu, Chih-Hung, Shen, Ying-Chun, Wang, Tsang-En, Li, Chung-Pin, Chen, Ming-Huang, Kao, Wei-Yao, Chang, Ping-Ying, Wu, Cheng-Chung, Teng, Chien-Lin, Lu, Chang-Hsien, Lin, Shyh-Jer, Wang, Being-Whey, Chen, Yen-Yang, Chin, Yung-Hsin, Chung, Tsai-Rong, Yu, Wei-Lan, Lee, Mei-Hua, Lin, Ling-Fang, Lin, Pei-Chyi, Wu, Ya-Ling, Wang, Hui-Ling, Lu, Li-Ju, Chen, Shiang-Yi, Wu, Chih-Chu, and Wei, Te-Chih

Published
2015
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11. Safety and efficacy of anti-PD-1 inhibitor ABBV-181 in lung and head and neck carcinoma

Author

Italiano, A., primary, Cassier, P., additional, Roda, D., additional, Lin, C.-C., additional, Peltola, K., additional, Gazzah, A., additional, Shiah, H.-S., additional, Calvo, E., additional, Tosi, D., additional, Gao, B., additional, warburton, L., additional, Tanner, M., additional, Englert, S., additional, Lambert, S., additional, Parikh, A., additional, Afar, D., additional, Vosganian, G., additional, and Moreno, V., additional

Published
2019
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15. Oral paclitaxel and HM30181A demonstrate clinical activity in metastatic breast cancer (MBC) patients

Author

Dai, M.-S., primary, Chao, T.-Y., additional, Chao, T.-C., additional, Chiu, C.-F., additional, Lu, Y.-S., additional, Shiah, H.-S., additional, Wu, Y.-Y., additional, Gerald Fetterly, G., additional, Hung, N., additional, Cutler, D.L., additional, Kwan, R., additional, Douglas Kramer, D., additional, Chan, W.-K., additional, and Hung, T., additional

Published
2018
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23. Effective sirolimus treatment for refractory spindle cell haemangioma.

Author

Ho CB, Hsieh K, Chen WY, Lin YT, Chiou JF, Lee HL, and Shiah HS

Subjects
Adult, Dose-Response Relationship, Drug, Drug Administration Schedule, Female, Hand, Hemangioma pathology, Humans, Neoplasm Recurrence, Local pathology, Skin blood supply, Skin pathology, Skin Neoplasms pathology, TOR Serine-Threonine Kinases antagonists & inhibitors, Treatment Outcome, Hemangioma drug therapy, Neoplasm Recurrence, Local drug therapy, Sirolimus administration & dosage, Skin Neoplasms drug therapy
Published
2018
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24. Pseudomonas exotoxin A-epidermal growth factor (EGF) mutant chimeric protein as an indicator for identifying amino acid residues important in EGF-receptor interaction.

Author

Shiah HS, Chen TY, Chang CM, Chow JT, Kung HJ, and Hwang J

Subjects
Amino Acid Sequence, Base Sequence, Cell Line, Cell Survival drug effects, Cloning, Molecular, Epidermal Growth Factor genetics, Epidermal Growth Factor pharmacology, Escherichia coli genetics, Exotoxins genetics, Exotoxins pharmacology, Humans, Molecular Sequence Data, Mutagenesis, Site-Directed, Plasmids, Pseudomonas aeruginosa genetics, Pseudomonas aeruginosa metabolism, Recombinant Fusion Proteins pharmacology, Pseudomonas aeruginosa Exotoxin A, ADP Ribose Transferases, Bacterial Toxins, Epidermal Growth Factor metabolism, ErbB Receptors metabolism, Exotoxins metabolism, Recombinant Fusion Proteins metabolism, Virulence Factors
Abstract

Epidermal growth factor (EGF) was fused to the carboxyl end of a modified pseudomonas exotoxin A that has its toxin binding domain deleted. This chimeric toxin designated as PE(delta Ia)-EGF kills A431 cells through the EGF receptor-mediated pathway. In this study, we used a random mutagenesis approach to make point mutations on EGF, followed by replacing the wild type EGF in PE(delta Ia)-EGF with these EGF mutants. We have constructed 14 different PE(delta Ia)-EGFmutants, and examined their EGF receptor binding activity as well as their cytotoxicity to A431 cells. Our results showed that individual mutations of Val19 to Glu and Val34 to Asp in the EGF domain of PE(delta Ia)-EGFmutants resulted in an increase in the binding affinity to EGF receptor and cytotoxicity to A431 cells. On the other hand, individual mutations of His16 to Asp and Gly18 to Ala in the EGF domain of PE(delta Ia)-EGFmutants lead to a decrease in the binding affinity to EGF receptor and cytotoxicity to A431 cells. In addition, mutations of any of the cysteine residues of EGF in PE(delta Ia)-EGFmutants resulted in the loss of their binding activity to EGF receptor and a corresponding loss of their cytotoxicity. This study indicates that the cytotoxicity of PE(delta Ia)-EGFmutant to EGF receptor-bearing cells may be used as an indicator to screen mutations of EGF important in EGF-receptor interactions.

Published
1992

25. Effect of ethanol on hepatotoxicity and hepatic DNA-binding of aflatoxin B1 in rats.

Author

Wang CJ, Wang SW, Shiah HS, and Lin JK

Subjects
Aflatoxin B1, Aflatoxins toxicity, Animals, Drug Synergism, Glutathione analysis, Glutathione physiology, Glutathione Peroxidase analysis, Glutathione Transferase analysis, Liver metabolism, Male, Rats, Rats, Inbred Strains, Aflatoxins metabolism, Carcinogens metabolism, DNA metabolism, Ethanol toxicity, Liver drug effects
Abstract

The hepatocarcinogen aflatoxin B1 is converted to reactive metabolites that bind covalently to cellular macromolecules. These metabolites may also react with glutathione, resulting in the formation of glutathione conjugates and detoxication of the reactive metabolite. When rats were pretreated with ethanol by gastric intubation at a dose of 100 mmol/kg, 6 hr (the time of maximal GSH depletion) before the administration of aflatoxin B1, the covalent binding of 8,9-epoxide-aflatoxin B1 to DNA in vivo was increased by 47% and the hepatotoxicity was also potentiated. However, the covalent binding was not increased by pretreatment with ethanol 18 hr (time with approximately normal GSH levels) before administration of the toxin, and no potentiation of hepatotoxicity was observed. Pretreatment with a non-toxic dose of ethanol had no effects on the activity of glutathione S-transferase and glutathione peroxidase. These results suggest that the depletion of GSH and the increased formation of DNA-adduct from the liver constitute an important mechanism for the potentiation of aflatoxin B1-induced hepatotoxicity by ethanol.

Published
1990
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