Te-Sheng Chang
Memorial Hospital of South Bend
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Featured researches published by Te-Sheng Chang.
Journal of Biomedical Science | 2014
Yung-Yu Hsieh; Chien-Heng Shen; Wen-Shih Huang; Chih-Chien Chin; Yi-Hung Kuo; Meng Chiao Hsieh; Hong-Ren Yu; Te-Sheng Chang; Tseng-Hsi Lin; Yung-Wei Chiu; Hsing-Chun Kuo; Shui-Yi Tung
BackgroundStromal cell-derived factor-1 (SDF-1) (CXC chemokine ligand-12)/CXC chemokine receptor 4 (CXCR4) is involved in the carcinogenesis of human gastric cancer, where it stimulates angiogenesis and favors metastasis of tumor cells to distant organs. In addition, resistin is suggested to be an important link between obesity and the development of gastric cancer. Resistin has identified as an important player in inflammatory responses, and emerged as a mediator in inflammation-associated cancer. A limited number of studies have investigated the association of resistin and SDF-1 with gastric cancer. Herein, we investigated the molecular mechanisms by which resistin influences the expression of SDF-1 in gastric carcinoma cells.ResultsHuman gastric cancer cell lines were exposed to doses of resistin; SDF-1 expression and secretion levels were then determined. Real-time polymerase chain reaction and western blotting analyses were performed to clarify molecular changes. Inhibition of Toll-like receptor 4 (TLR4) by a competitive antagonist inhibited resistin-induced SDF-1 expression. Pharmacological inhibitors and small interfering RNA (siRNA) demonstrated that activation of the p38 mitogen-activated protein kinase (MAPK) pathway is critical for resistin-induced SDF-1 expression mediated by TLR4. The promoter activity and transcription factor enzyme-linked immunosorbent assay revealed that resistin induced expression of SDF-1 mediated by NF-κB in gastric cancer cells. Inhibition of p38 MARK activation blocked the SDF-1-induced expression and the SDF-1 promoter activity in the cancer gastric cells. Chromatin immunoprecipitation assay revealed that inhibition of p38 MARK activation also blocked the resistin-increased NF-κB-DNA-binding activity.ConclusionsResistin-induced SDF-1 upregulation by activation of TLR4, p38 MARK and NF-κB may explain a new role of resistin in the link of obesity and gastric cancer.
Journal of Clinical Gastroenterology | 2008
I-Lin Lee; Cheng-Shyong Wu; Shui-Yi Tung; Paul Y. Lin; Chien-Hung Shen; Kuo-Ling Wei; Te-Sheng Chang
Goal To evaluate the efficacy of endoscopic submucosal dissection (ESD) for early gastric cancers (EGCs) at a new endoscopic center. Background ESD is a novel technique that can facilitate en-bloc resection of EGCs, but seldom reported outside Japan. Study A total of 25 consecutive patients (25 lesions) underwent ESD from June 2004 to March 2006. Patients were divided into 2 groups: group A underwent ESD from June 2004 to May 2005 (introduction stage) and group B from June 2005 to March 2006. The following data were obtained: tumor size, tumor location, operative time, and major complication. Results The complete resection was achieved in 20 lesions (success rate 80%). Four out of 10 lesions from group A were removed by conventional endoscopic mucosal resection (EMR) piecemeally after ESD failure. Conversely, 14 patients from group B (n=15) were resected by ESD en-bloc (success rate 93.3%). One patient with microscopic residual tumor after ESD was further treated by surgical resection. The time required for resection was significantly longer in group A when compared with group B (130.5 min vs. 81.5 min, P<0.05). Postoperative complication rate between the 2 groups were similar. One patient with piecemeal EMR recurred in follow-up, and was further treated successfully by EMR. Conclusions ESD is an ideal method for EGC treatment, but it may result in a risk of complication. The complete resection rate can be improved by endoscopists experience. Sophisticated endoscopic hemostasis and clipping skills are essential prior ESD procedures. Conventional EMR techniques are also obligatory during the beginning period.
International Journal of Molecular Sciences | 2017
Te-Sheng Chang; Kuo-Liang Wei; Chung-Kuang Lu; Yi-Hsing Chen; Ying-Tung Cheng; Shui-Yi Tung; Cheng-Shyong Wu; Ming-Ko Chiang
The aberrant activation of Wnt signaling has been implicated in a variety of human cancers, including gastric cancer. Given the current hypothesis that cancer arises from cancer stem cells (CSCs), targeting the critical signaling pathways that support CSC self-renewal appears to be a useful approach for cancer therapy. Cell cycle and apoptosis regulator 1 (CCAR1) is a transcriptional coactivator which has been shown to be a component of Wnt/β-catenin signaling, and which plays an important role in transcriptional regulation by β-catenin. However, the function and clinical significance of CCAR1 in gastric cancer have not been elucidated. Here, we show that elevated CCAR1 nuclear expression correlates with the occurrence of gastric cancer. In addition, RNAi-mediated CCAR1 reduction not only suppressed the cell growth and increased apoptosis in AGS and MKN28 cells, but also reduced the migration and invasion ability of these cells. Furthermore, an in vivo xenograft assay revealed that the expression level of CCAR1 was critical for tumorigenesis. Our data demonstrates that CCAR1 contributes to carcinogenesis in gastric cancer and is required for the survival of gastric cancer cells. Moreover, CCAR1 may serve as a diagnostic marker and a potential therapeutic target.
Advances in Digestive Medicine | 2015
Yung-Yu Hsieh; I-Lin Lee; Kuo-Liang Wei; Te-Sheng Chang; Shui-Yi Tung; Cheng-Shyong Wu; Yi-Hsiung Lin
Limited data are available on the interval of disease‐free status after endoscopic submucosal dissection (ESD) for early gastric cancer and precancer lesion in Taiwan. In this long‐term (2–105 months) follow‐up study, we analyzed the risk factors that affect the local recurrence and noncurative resection (non‐CR) of these lesions.
International Journal of Colorectal Disease | 2007
Wen-Shih Huang; Paul Y. Lin; Chih-Chien Chin; Chung-Hung Yeh; Ching-Chuan Hsieh; Te-Sheng Chang; Jeng-Yi Wang
World Journal of Surgical Oncology | 2016
Wei-Ming Chen; Kuo-Liang Wei; Yi-Shing Chen; Pey-Jium Chang; Shui-Yi Tung; Te-Sheng Chang; Hao-Chun Huang; Chein-Heng Shen; Yung-Yu Hsieh; Cheng-Shyong Wu
The American Journal of Gastroenterology | 2016
Te-Sheng Chang; Yu-Chih Wu; Shui-Yi Tung; Kuo-Liang Wei; Yung-Yu Hsieh; Hao-Chun Huang; Wei-Ming Chen; Chien-Heng Shen; Chang-Hsien Lu; Cheng-Shyong Wu; Ying-Huang Tsai; Yen Hua Huang
Archive | 2015
Te-Sheng Chang; Yu-Chih Wu; Shui-Yi Tung; Kuo-Liang Wei; Yung-Yu Hsieh; Hao-Chun Huang; Wei-Ming Chen; Chien-Heng Shen; Chang-Hsien Lu; Cheng-Shyong Wu; Ying-Huang Tsai; Yen Hua Huang
International Journal of Rheumatic Diseases | 2018
Ko-Ming Lin; Wei-Ming Chen; Shui-Yi Tung; Kuo-Liang Wei; Chein-Heng Shen; Te-Sheng Chang; Pey-Jium Chang
Cancer Research | 2018
Ssu-Chuan Lai; Te-Sheng Chang; Yu-Ting Su; Yu-Chih Wu; Yung-Che Kuo; Pei-Chi Lan; Yen-Hua Huang