Article
Medicine, General & Internal
Yoshiaki Usui, Yukari Taniyama, Mikiko Endo, Yuriko N. Koyanagi, Yumiko Kasugai, Isao Oze, Hidemi Ito, Issei Imoto, Tsutomu Tanaka, Masahiro Tajika, Yasumasa Niwa, Yusuke Iwasaki, Tomomi Aoi, Nozomi Hakozaki, Sadaaki Takata, Kunihiko Suzuki, Chikashi Terao, Masanori Hatakeyama, Makoto Hirata, Kokichi Sugano, Teruhiko Yoshida, Yoichiro Kamatani, Hidewaki Nakagawa, Koichi Matsuda, Yoshinori Murakami, Amanda B. Spurdle, Keitaro Matsuo, Yukihide Momozawa
Summary: This study reveals that certain genetic variants associated with Helicobacter pylori infection can increase the risk of gastric cancer. Individuals carrying these genetic variants and infected with H. pylori have an even higher risk of developing gastric cancer.
NEW ENGLAND JOURNAL OF MEDICINE
(2023)
Review
Biochemistry & Molecular Biology
Silvia Salvatori, Irene Marafini, Federica Laudisi, Giovanni Monteleone, Carmine Stolfi
Summary: H. pylori infection contributes to the onset and development of gastric cancer through the mechanisms of chronic inflammation and DNA damage to gastric epithelial cells.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2023)
Article
Biochemistry & Molecular Biology
So Dam Lee, Haengdueng Jeong, Bo Ram Hwang, Byeong Min Yu, Yejin Cho, Ki Teak Nam, Hyunki Kim, Yong Chan Lee
Summary: Strains of Helicobacter pylori positive for CagA may contribute to the development of gastric cancer through the induction of CK2 activation and CK28 degradation. The downregulation of CK28 and subsequent activation of AKT and Snail signaling pathways may play a crucial role in the epithelial-to-mesenchymal transition (EMT) in gastric cancer. CK2 could be a potential molecular target for the treatment of H. pylori-infected gastric cancer.
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE
(2023)
Article
Plant Sciences
Qin Tang, Zhengcai Ma, Xiang Tang, Yan Liu, Huimin Wu, Yu Peng, Baihua Jiao, Rui Wang, Xiaoli Ye, Hang Ma, Xuegang Li
Summary: The study aimed to find the most effective alkaloid against Helicobacter pylori in Rhizoma Coptidis and illustrate the probable mechanisms. The results showed that coptisine was the most effective alkaloid against H. pylori and could eradicate the bacteria through multiple mechanisms while reducing inflammation.
JOURNAL OF ETHNOPHARMACOLOGY
(2023)
Review
Oncology
Michelle C. C. Lim, Phatcharida Jantaree, Michael Naumann
Summary: Helicobacter pylori is a pathogenic bacterium that resides in the stomach lining and causes inflammation called type B gastritis. The chronic inflammation induced by H. pylori and other factors may lead to the development of stomach neoplasms and adenocarcinoma. Dysregulation of cellular processes in the stomach lining and microenvironment is a characteristic of H. pylori infection. In this review, we discuss the contradictory role of H. pylori in promoting or suppressing apoptosis in gastric epithelial cells and highlight the key processes in the microenvironment that contribute to apoptosis and gastric carcinogenesis.
Article
Oncology
Jun Sun, Hui Cao, Tingting Wen, Zi Xu, Xian Zhang, Jianjun Wang, Hong Zhu
Summary: This study investigated the expression and functions of CD59 in H. pylori infected gastric cancer (GC). The results showed that H. pylori infection significantly decreased the expression of CD59 in GC cells and tissues. CD59 expression was linked to the survival rate of GC patients and affected various immune cells in the immune microenvironment of GC.
Article
Oncology
Mahjerin Nasrin Reza, Shahin Mahmud, Nadim Ferdous, Ishtiaque Ahammad, Mohammad Uzzal Hossain, Md. Al Amin, A. K. M. Mohiuddin
Summary: In this study, two siRNA molecules were designed to silence the CagA and VacA genes of H. pylori, which are significantly involved in gastric cancer development. These designed siRNAs should effectively silence the CagA and VacA genes during siRNA mediated treatment in gastric cancer.
Editorial Material
Microbiology
Agustina Taglialegna
Summary: In this study, Sharafutdinov et al. report the identification of a single nucleotide polymorphism in the gene encoding the HtrA protease of Helicobacter pylori that is linked to gastric cancer.
NATURE REVIEWS MICROBIOLOGY
(2023)
Article
Multidisciplinary Sciences
Tomohiko Yasuda, Hyun Seok Lee, Su Youn Nam, Hiroto Katoh, Yuko Ishibashi, Somay Yamagata Murayama, Hidenori Matsui, Hiroki Masuda, Emiko Rimbara, Nobuyuki Sakurazawa, Hideyuki Suzuki, Hiroshi Yoshida, Yasuyuki Seto, Shumpei Ishikawa, Seong Woo Jeon, Masahiko Nakamura, Sachiyo Nomura
Summary: Genetic analysis and culturing techniques for gastric non-Helicobacter pylori Helicobacter (NHPH) are advancing, with NHPH reported to accompany certain gastric conditions. A study on Korean gastric cancer patients found a low percentage positive for NHPH, suggesting it may play a role in gastric cancer development, albeit with lower pathogenicity compared to H. pylori.
SCIENTIFIC REPORTS
(2022)
Article
Immunology
Rui M. Ferreira, Joana Figueiredo, Ines Pinto-Ribeiro, Irene Gullo, Dionyssios N. Sgouras, Laura Carreto, Patricia Castro, Manuel A. Santos, Fatima Carneiro, Raquel Seruca, Ceu Figueiredo
Summary: Helicobacter pylori infection induces overexpression of laminin gamma 2 in gastric cancer cells, promoting cell invasion and resistance to apoptosis through modulation of Src, JNK, and AKT activity. Laminin gamma 2 and its downstream effectors could be potential therapeutic targets, and H. pylori eradication may delay the onset and progression of gastric cancer.
JOURNAL OF INFECTIOUS DISEASES
(2022)
Article
Public, Environmental & Occupational Health
Pang Yao, Christiana Kartsonaki, Julia Butt, Rima Jeske, Catherine de Martel, Martyn Plummer, Yu Guo, Sarah Clark, Robin G. Walters, Yiping Chen, Daniel Avery, Jun Lv, Canqing Yu, Hao Wang, Michael Hill, Richard Peto, Liming Li, Tim Waterboer, Zhengming Chen, Iona Y. Millwood, Ling Yang
Summary: This study found that Helicobacter pylori infection is associated with the risk of non-cardia gastric cancer (NCGC) and cardia gastric cancer (CGC). There is uncertainty about the associations between sero-positivity to different H. pylori antigens and the risk of NCGC and CGC in different populations.
INTERNATIONAL JOURNAL OF EPIDEMIOLOGY
(2023)
Article
Biochemistry & Molecular Biology
Rejina Shrestha, Naoko Murata-Kamiya, Satoshi Imai, Masami Yamamoto, Tetsuya Tsukamoto, Sachiyo Nomura, Masanori Hatakeyama
Summary: The initial step in bacterial infection is the adherence of the bacterium to the target cell surface. This study found that the mouse stomach has a much lower expression level of Ceacam1 compared to the human stomach, which leads to the inability of the bacteria to deliver the CagA protein due to the lack of interaction between HopQ and Ceacam1 in mouse gastric epithelial cells.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2022)
Article
Food Science & Technology
Aina Ichihara, Hinako Ojima, Kazuyoshi Gotoh, Osamu Matsushita, Susumu Take, Hiroyuki Okada, Akari Watanabe, Kenji Yokota
Summary: This study aimed to explore the association between different antibody reactivities and bacterial genome organization. High-reactive strains showed high gene homology, while inversion around the vacA gene was found in the genome of poorly responsive antigen strains.
Article
Biochemical Research Methods
Lusheng Song, Minkyo Song, Charles S. Rabkin, Stacy Williams, Yunro Chung, Jennifer Van Duine, Linda M. Liao, Kailash Karthikeyan, Weimin Gao, Jin G. Park, Yanyang Tang, Jolanta Lissowska, Ji Qiu, Joshua LaBaer, M. Constanza Camargo
Summary: This study evaluated humoral responses to a nearly complete H. pylori immunoproteome among GC cases and controls, finding higher prevalence of certain antibodies in controls and lower seroprevalence in GC cases, suggesting immune protection and potential changes in specific proteins.
JOURNAL OF PROTEOME RESEARCH
(2021)
Review
Oncology
Naoko Murata-Kamiya, Masanori Hatakeyama
Summary: Infection with cagA-positive Helicobacter pylori strains can lead to the development of gastric cancer and is associated with genomic changes in host cells. Inside the host cells, the CagA protein interacts with multiple host cell proteins, disrupting normal cell signaling. H. pylori infection also causes DNA damage and affects DNA repair mechanisms. Once driver gene mutations occur, H. pylori CagA is no longer necessary for gastric carcinogenesis.