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Nai Wen Chang
Researcher at China Medical University (Taiwan)
Publications - 14
Citations - 469
Nai Wen Chang is an academic researcher from China Medical University (Taiwan). The author has contributed to research in topics: Cancer & Fenofibrate. The author has an hindex of 10, co-authored 14 publications receiving 405 citations.
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Journal ArticleDOI
Functional Genomic Analysis Identified Epidermal Growth Factor Receptor Activation as the Most Common Genetic Event in Oral Squamous Cell Carcinoma
Jim Jinn-Chyuan Sheu,Chun Hung Hua,Lei Wan,Ying Ju Lin,Ming Tsung Lai,Hsien Chang Tseng,Natini Jinawath,Ming Hsui Tsai,Nai Wen Chang,Chin Fen Lin,Chyi-Chyang Lin,Lie Jiau Hsieh,Tian Li Wang,Ie Ming Shih,Fuu Jen Tsai +14 more
TL;DR: The data suggest that EGFR signaling is important in oral cancer development and that anti-EGFR therapy would benefit patients who carry the 7p11.2 amplicon in their tumors.
Journal ArticleDOI
Co-treating with arecoline and 4-nitroquinoline 1-oxide to establish a mouse model mimicking oral tumorigenesis.
Nai Wen Chang,Ren Jeng Pei,Hsien Chang Tseng,Kun Tu Yeh,Hsu Chin Chan,Miau Rong Lee,Chingju Lin,Wen Tsong Hsieh,Ming-Ching Kao,Ming Hsui Tsai,Chin Fen Lin +10 more
TL;DR: Data subsequently attained from this mouse model support a role for alphaB-crystallin and Hsp27 as clinical markers for tumor progression and the study of the promoting effects of arecoline on tongue tumorigenesis.
Journal Article
Association of XRCC4 codon 247 polymorphism with oral cancer susceptibility in Taiwan.
Hsien Chang Tseng,Ming Hsui Tsai,Chang Fang Chiu,Chung Hsing Wang,Nai Wen Chang,Chih Yang Huang,Chia Wen Tsai,Chia Wen Tsai,Shiu Yun Liang,Cheng Li Wang,Da Tian Bau +10 more
TL;DR: The results provide the first evidence that the heterozygous A allele of the XRCC4 codon 247 may be associated with the development of oral cancer and may be a novel useful marker for primary prevention and anticancer intervention.
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AMPK-dependent signaling modulates the suppression of invasion and migration by fenofibrate in CAL 27 oral cancer cells through NF-κB pathway
Shih Chang Tsai,Ming Hsui Tsai,Chang Fang Chiu,Chi Cheng Lu,Sheng-Chu Kuo,Nai Wen Chang,Jai Sing Yang +6 more
TL;DR: Fenofibrate considerably inhibited metastatic behaviors of CAL 27 cells might be mediated through blocking NF‐κB signaling, resulting in the inhibition of MMPs; these effects were AMPK‐dependent rather than PPARα signaling.
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Fenofibrate Suppresses Oral Tumorigenesis via Reprogramming Metabolic Processes: Potential Drug Repurposing for Oral Cancer.
TL;DR: The present study demonstrates that fenofibrate provided novel mechanisms for delaying oral tumor development via the reprogramming of metabolic processes, and provides a molecular rationale whereby fen ofibrate exerts anticancer and additional beneficial effects for the treatment of oral cancer patients.