Hsiu-Chi Cheng, MD, PhD
E-mail:teishuki@mail.ncku.edu.tw
TEL:06-2353535 ext 4733 FAX:06-302816
Educations / Professional Experience |
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Educations |
2003-2009 |
Ph.D., Institute of Clinical Medicine, National Cheng Kung University |
1989-1996 |
M.D., School of Medicine, China Medical College |
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Current Position |
2019- |
Professor in Department of Internal Medicine, National Cheng Kung University, Tainan |
2020- |
Vice Dean, Tainan hospital, Ministry of Health and Welfare |
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Professional Experience |
2014-2019 |
Associate Professor in Department of Internal Medicine, National Cheng Kung University, Tainan |
2010–2014 |
Assistant Professor in Department of Internal Medicine, National Cheng Kung University, Tainan |
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2007-2010 |
Adjunct Assistant Professor in Department of Internal Medicine, National Cheng Kung University Hospital, Tainan |
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2007-2020 |
Head in Division of General Internal Medicine, National Cheng Kung University Hospital, Tainan |
Expertise /Research Interests |
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Diagnosis and treatment of upper gastrointestinal tract, Gastric precancerous conditions, The pathogenesis of H. pylori infection, The gastrointestinal microbiome |
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Research Interests |
Gastric cancer is the 6th most common cancer and the 3rd most common cause of cancer death in the world and H. pylori is the major factor to induce gastric cancer. I participate in the Helicobacter pylori study group to study the pathogenic and carcinogenic mechanisms of the host and bacteria. Regarding to host, we devised the original corpus-predominant gastritis index (CGI) according to gastric pathology and found that it could be an early marker for identifying who are at risk of gastric cancer among first-degree gastric cancer family and H. pylori-infected non-ulcer dyspepsia subjects. Additionally, we have enrolled about 500 H. pylori-infected subjects and their gastric tissues before and after eradicating H. pylori and followed up them for 3 to 20 years. We explored the disease evolution of precancerous conditions according to the pathologies after eradicating H. pylori and found the incidence rates of gastric cancer in each stage at baseline. These findings could provide physicians that who, when, and how should receive surveillance endoscopy to diagnose gastric cancer at early stage. Among these patients, some had regression of precancerous conditions, but the others did not. The reasons should be further studied. Thus, these data will be the materials to answer the questions. Currently, I and our group conduct a human microbiology project sponsored by Ministry of Science and Technology (MOST). One part of the project is to explore the role of gastric microbiota in patients who did not have regress of precancerous conditions after eradicating H. pylori.
Regarding the bacteria, H. pylori binds integrin α5β1 of host gastric epithelial cells via the type-IV secretion system (T4SS) to deliver CagA protein into cells. CagA protein stimulates host cells to secrete IL-8 and suppresses apoptosis to induce carcinogenesis. H. pylori CagL protein is an adhesion subunit of T4SS and we found that the amino acid polymorphism of Y58/E59 of CagL increases the risk of gastric cancer by 4.6 times. Additionally, H. pylori ImaA protein degrades the host integrin β1 and antagonizes the interaction between H. pylori T4SS and integrin α5β1. Because only 30% of H. pylori strains could translocate CagA into host cells, it is intriguing to study the amino acid polymorphism of ImaA protein to regulate the interaction between T4SS and integrin α5β1 and induce gastritis and precancerous conditions. Currently, I conduct a MOST project to answer these questions. |
Research Directions |
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