Gastric Carcinogenesis

2018 ◽  
pp. 51-62
Author(s):  
Hitoshi Tsugawa ◽  
Hidekazu Suzuki
Keyword(s):  
Gastric Carcinogenesis

Defects in TGF beta signaling by smad 4 and ELF spectrins are associated with gastric carcinogenesis

2001 ◽  
Vol 120 (5) ◽  
pp. A495-A495
Author(s):  
Y GANG ◽  
S DANOVITCH ◽  
T FLEURY ◽  
B MISHRA ◽  
C DENG ◽  
...  
Keyword(s):  
Gastric Carcinogenesis ◽  
Tgf Beta

In Vitro Evidence of the Role of COX-2 in Attenuating Gastric Inflammation and Promoting Gastric Carcinogenesis

2002 ◽  
Vol 21 (2) ◽  
pp. 12 ◽  
Author(s):  
Ki-Baik Hahm ◽  
Ho-Yeong Lim ◽  
Seonghyang Sohn ◽  
Hyuk-Jae Kwon ◽  
Ki-Myung Lee ◽  
...  
Keyword(s):  
Gastric Carcinogenesis ◽  
Cox 2

Changes of the Gastric Mucosal Microbiome Associated with Histological Stages of Gastric Carcinogenesis

2019 ◽  
Author(s):  
Yunsheng Yang ◽  
Zikai Wang ◽  
Xuefeng Gao ◽  
Ranran Zeng ◽  
Qiong Wu ◽  
...  
Keyword(s):  
Gastric Carcinogenesis

scholarly journals Circ_SMAD4 promotes gastric carcinogenesis by activating wnt/β‐catenin pathway

2021 ◽  
Author(s):  
Liyan Wang ◽  
Bin Li ◽  
Xiaoyuan Yi ◽  
Xuhua Xiao ◽  
Qinghua Zheng ◽  
...  
Keyword(s):  
Gastric Carcinogenesis

Gastric microbiome profile throughout gastric carcinogenesis: beyond helicobacter

2021 ◽  
pp. 1-9
Author(s):  
Pedro Pimentel-Nunes ◽  
António Barros ◽  
Inês Pita ◽  
Isabel Miranda ◽  
Glória Conceição ◽  
...  
Keyword(s):  
Gastric Carcinogenesis ◽  
Microbiome Profile

scholarly journals Gastric Cancer Microbiome

Pathobiology ◽  
2021 ◽  
Vol 88 (2) ◽  
pp. 156-169
Author(s):  
Williams Fernandes Barra ◽  
Dionison Pereira Sarquis ◽  
André Salim Khayat ◽  
Bruna Cláudia Meireles Khayat ◽  
Samia Demachki ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Small Sample Size ◽  
Total Sample ◽  
Clinical Situation ◽  
Gastric Carcinogenesis ◽  
Comprehensive Analysis ◽  
Small Sample ◽  
Metagenomic Data ◽  
Clinical Scenarios ◽  
H Pylori

Identifying a microbiome pattern in gastric cancer (GC) is hugely debatable due to the variation resulting from the diversity of the studied populations, clinical scenarios, and metagenomic approach. <i>H. pylori</i> remains the main microorganism impacting gastric carcinogenesis and seems necessary for the initial steps of the process. Nevertheless, an additional non-<i>H. pylori</i> microbiome pattern is also described, mainly at the final steps of the carcinogenesis. Unfortunately, most of the presented results are not reproducible, and there are no consensual candidates to share the <i>H. pylori</i> protagonists. Limitations to reach a consistent interpretation of metagenomic data include contamination along every step of the process, which might cause relevant misinterpretations. In addition, the functional consequences of an altered microbiome might be addressed. Aiming to minimize methodological bias and limitations due to small sample size and the lack of standardization of bioinformatics assessment and interpretation, we carried out a comprehensive analysis of the publicly available metagenomic data from various conditions relevant to gastric carcinogenesis. Mainly, instead of just analyzing the results of each available publication, a new approach was launched, allowing the comprehensive analysis of the total sample amount, aiming to produce a reliable interpretation due to using a significant number of samples, from different origins, in a standard protocol. Among the main results, <i>Helicobacter</i> and <i>Prevotella</i> figured in the “top 6” genera of every group. <i>Helicobacter</i> was the first one in chronic gastritis (CG), gastric cancer (GC), and adjacent (ADJ) groups, while <i>Prevotella</i> was the leader among healthy control (HC) samples. Groups of bacteria are differently abundant in each clinical situation, and bacterial metabolic pathways also diverge along the carcinogenesis cascade. This information may support future microbiome interventions aiming to face the carcinogenesis process and/or reduce GC risk.

Action of vinblastine on experimental gastric carcinogenesis

1986 ◽  
Vol 101 (6) ◽  
pp. 833-837
Author(s):  
V. K. Gurkalo ◽  
N. I. Vol'fson
Keyword(s):  
Gastric Carcinogenesis

Original Article: MicroRNA Dysregulation in the Gastric Carcinogenesis Cascade: Can We Anticipate Its Role in Individualized Care?

Pathobiology ◽  
2021 ◽  
pp. 1-13
Author(s):  
Inês Pita ◽  
Diogo Libânio ◽  
Francisca Dias ◽  
Ana Luísa Teixeira ◽  
Inês Nogueira ◽  
...  
Keyword(s):  
Tissue Expression ◽  
Normal Mucosa ◽  
Cross Sectional Study ◽  
Gastric Carcinogenesis ◽  
Endoscopic Biopsy ◽  
Cross Sectional ◽  
Oncogenic Potential ◽  
Individualized Care ◽  
Gastric Neoplasia ◽  
Microrna Dysregulation

<b><i>Background:</i></b> Gastric carcinogenesis progresses from normal mucosa, atrophic/metaplastic gastritis, and dysplasia to adenocarcinoma. MicroRNAs (miRNAs) regulate DNA expression and have been implicated; however, their role is not fully established. <b><i>Aims:</i></b> The aim of this study was to characterize plasma and tissue expression of several miRNAs in gastric carcinogenesis stages. <b><i>Methods:</i></b> Single-center cross-sectional study in 64 patients: 19 controls (normal mucosa); 15 with extensive atrophic/metaplastic gastritis; and 30 with early gastric neoplasia (EGN). Seven miRNAs (miR-21, miR-146a, miR-181b, miR-370, miR-375, miR 181b, and miR-490) were quantified by real time-qPCR in peripheral blood and endoscopic biopsy samples. <b><i>Results:</i></b> We found a significant upregulation of miR-181b, miR-490, and miR-21 in the EGN mucosa (overexpression 2–14-times higher than controls). We observed a significant underexpression of miR-146a and miR-370 in atrophic/metaplastic gastritis (86 and 66% decrease, <i>p</i> = 0.008 and <i>p</i> = 0.001) and in EGN (89 and 62% reduction, <i>p</i> = 0.034 and <i>p</i> = 0.032) compared with controls. There were no differences between lesions and nonneoplastic mucosa and no dysregulation of plasma miRNAs. <b><i>Conclusion:</i></b> We found significant dysregulation of 5 miRNAs in gastric carcinogenesis, suggesting a tumor suppressor role for miR-146a and miR-370 and oncogenic potential for miR-21, miR-181, and miR-490. These changes happen diffusely in the gastric mucosa, suggesting a high-risk field defect, which may influence these patients’ surveillance.

scholarly journals Helicobacter pylori Induces a Novel NF-kB/LIN28A/let-7a/hTERT Axis to Promote Gastric Carcinogenesis

2020 ◽  
Vol 19 (1) ◽  
pp. 74-85
Author(s):  
Li Shen ◽  
Jiping Zeng ◽  
Lin Ma ◽  
Shuyan Li ◽  
Chunyan Chen ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Gastric Carcinogenesis
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