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  4. Sorafenib enhances radiation-induced apoptosis in hepatocellular carcinoma by inhibiting STAT3
 
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Sorafenib enhances radiation-induced apoptosis in hepatocellular carcinoma by inhibiting STAT3

Journal
International journal of radiation oncology, biology, physics
Journal Volume
86
Journal Issue
3
Date Issued
2013-07-01
Author(s)
CHAO YUAN HUANG  
Lin, Chen-Si
Tai, Wei-Tien
Hsieh, Chi-Ying
Shiau, Chung-Wai
ANN-LII CHENG  
Chen, Kuen-Feng
DOI
10.1016/j.ijrobp.2013.01.025
URI
https://scholars.lib.ntu.edu.tw/handle/123456789/584719
URL
https://scholars.lib.ntu.edu.tw/handle/123456789/561255
Abstract
Hepatocellular carcinoma (HCC) is one of the most common and lethal human malignancies. Lack of efficient therapy for advanced HCC is a pressing problem worldwide. This study aimed to determine the efficacy and mechanism of combined sorafenib and radiation therapy treatment for HCC.
SDGs

[SDGs]SDG3

Other Subjects
Cell culture; Cell death; Cells; Cytology; Drug products; Enzyme inhibition; Radiotherapy; Signal transduction; Ectopic expressions; Hepatocellular carcinoma; Human malignancies; Methods and materials; Radiation resistance; Radiation therapy treatment; Radiation-induced apoptosis; Signaling pathways; Radiation; caspase 9; cyclin D1; mitogen activated protein kinase 1; mitogen activated protein kinase 3; protein BAD; protein Bax; protein mcl 1; sorafenib; STAT3 protein; survivin; antineoplastic agent; BIRC5 protein, human; carbanilamide derivative; cyclin D1; drug derivative; inhibitor of apoptosis protein; myeloid cell leukemia sequence 1 protein; nicotinamide; protein bcl 2; sorafenib; STAT3 protein; tumor protein; animal experiment; animal model; apoptosis; article; cancer growth; cancer resistance; cell culture; colony formation; controlled study; down regulation; drug efficacy; drug mechanism; G2 phase cell cycle checkpoint; genetic transfection; human; human cell; human tissue; in vitro study; in vivo study; ionizing radiation; liver cell carcinoma; mouse; nonhuman; priority journal; protein expression; radiation induced apoptosis; radiosensitivity; RNA interference; signal transduction; Western blotting; chemoradiotherapy; drug antagonism; drug effect; liver cell carcinoma; liver tumor; methodology; physiology; radiation dose; Antineoplastic Agents; Apoptosis; Carcinoma, Hepatocellular; Chemoradiotherapy; Cyclin D1; Humans; Inhibitor of Apoptosis Proteins; Liver Neoplasms; Neoplasm Proteins; Niacinamide; Phenylurea Compounds; Proto-Oncogene Proteins c-bcl-2; Radiation Tolerance; RNA Interference; STAT3 Transcription Factor
Type
journal article

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