Bile Acid–Microbiome Interaction Promotes Gastric Carcinogenesis-Reference-Cited by-同舟云学术

Bile Acid–Microbiome Interaction Promotes Gastric Carcinogenesis

Published:2022-03-14 Issue:16 Volume:9 Page:2200263
ISSN:2198-3844
Container-title:Advanced Science
language:en
Short-container-title:Advanced Science

Author:

Wang Shouli¹,Kuang Junliang¹,Zhang Hongwei²,Chen Wenlian³,Zheng Xiaojiao¹,Wang Jieyi¹,Huang Fengjie¹,Ge Kun¹,Li Mengci¹,Zhao Mingliang¹,Rajani Cynthia⁴,Zhu Jinshui⁵,Zhao Aihua¹,Jia Wei¹⁴⁶^ORCID

Affiliation:

1. Center for Translational Medicine and Shanghai Key Laboratory of Diabetes Mellitus Shanghai Jiao Tong University Affiliated Sixth People's Hospital Shanghai 200233 China

2. Department of Metabolic and Bariatric Surgery Shanghai Jiao Tong University Affiliated Sixth People's Hospital Shanghai 200233 China

3. Cancer Institute, Longhua Hospital Shanghai University of Traditional Chinese Medicine Shanghai 200233 China

4. Cancer Biology Program University of Hawaii Cancer Center Honolulu HI 96813 USA

5. Department of Gastroenterology Shanghai Jiao Tong University Affiliated Sixth People's Hospital Shanghai 200233 China

6. School of Chinese Medicine Hong Kong Baptist University Kowloon Tong Hong Kong 999077 China

Funder

National Natural Science Foundation of China

Natural Science Foundation of Shanghai

Publisher

Wiley

Subject

General Physics and Astronomy,General Engineering,Biochemistry, Genetics and Molecular Biology (miscellaneous),General Materials Science,General Chemical Engineering,Medicine (miscellaneous)

Link

https://onlinelibrary.wiley.com/doi/pdf/10.1002/advs.202200263

Reference56 articles.

1. Cancer statistics in China, 2015

2. Helicobacter pylori-Induced Signaling Pathways Contribute to Intestinal Metaplasia and Gastric Carcinogenesis

3. Bile reflux gastritis and intestinal metaplasia at the cardia

4. Bile Acid Promotes Intestinal Metaplasia and Gastric Carcinogenesis

5. Chemoprevention of glandular stomach carcinogenesis through duodenogastric reflux in rats by a COX-2 inhibitor

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