ReviewWorld journal of gastroenterology2016
Inflammatory microenvironment contributes to epithelial-mesenchymal transition in gastric cancer.
Review in World journal of gastroenterology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
49 citing papers in PubMed.
- Review
- CagA-dependent expression of anti-inflammatory cytokine IL-13 and TNFRSF member Fn14 inFrontiers in microbiology · 2026Article
- Revealing Potential Therapeutic Targets in Gastric Cancer through Inflammation and Protein-Protein Interaction Hub Networks.Journal of Cancer · 2025Article
- The oral-gut axis in chronic atrophic gastritis: current perspectives and integrated strategies.Frontiers in immunology · 2025Review
- Helicobacter pylori promotes gastric cancer progression by activating the TGF-β/Smad2/EMT pathway through HKDC1.Cellular and molecular life sciences : CMLS · 2024Article
- Poorly cohesive gastric cancer with increased epithelial‑mesenchymal transition is associated with a poor prognosis.Oncology letters · 2024Article
- Collagen synthase P4HA3 as a novel biomarker for colorectal cancer correlates with prognosis and immune infiltration.Heliyon · 2024Article
- Integrative analysis revealed a correlation of PIAS family genes expression with prognosis, immunomodulation and chemotherapy.European journal of medical research · 2024Article
- IL-17A in gastric carcinogenesis: good or bad?Frontiers in immunology · 2024Review
- Article
- Unveiling the immunomodulatory shift: Epithelial-mesenchymal transition Alters immune mechanisms of amniotic epithelial cells.iScience · 2023Article
- Automated Assessment of the Area of Infiltration by CD8Bulletin of experimental biology and medicine · 2023Article
- The Role of EMT-Related lncRNAs in Ovarian Cancer.International journal of molecular sciences · 2023Review
- The Roles of Innate Lymphoid Cells in the Gastric Mucosal Immunology and Oncogenesis of Gastric Cancer.International journal of molecular sciences · 2023Review
- Prevention of malignant digestive system tumors should focus on the control of chronic inflammation.World journal of gastrointestinal oncology · 2023Review
- Cytokine-Like Protein 1 (CYTL1) as a Key Target of M-Stage Immune Infiltration in Stomach Adenocarcinoma.BioMed research international · 2023Article
- Cancer-associated fibroblasts refine the classifications of gastric cancer with distinct prognosis and tumor microenvironment characteristics.Frontiers in oncology · 2023Article
- Epithelial-Mesenchymal Plasticity Induced by Discontinuous Exposure to TGFβ1 Promotes Tumour Growth.Biology · 2022Article
- Helicobacter pylori and gastric cancer: a lysosomal protease perspective.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2022Review
- Identification of key pathways and genes in vestibular schwannoma using bioinformatics analysis.Experimental and therapeutic medicine · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gastric cancer (GC) is the fifth most common malignancy in the world. The major cause of GC is chronic infection with Helicobacter pylori (H. pylori). Infection with H. pylori leads to an active inflammatory microenvironment that is maintained by immune cells such as T cells, macrophages, natural killer cells, among other cells. Immune cell dysfunction allows the initiation and accumulation of mutations in GC cells, inducing aberrant proliferation and protection from apoptosis. Meanwhile, immune cells can secrete certain signals, including cytokines, and chemokines, to alter intracellular signaling pathways in GC cells. Thus, GC cells obtain the ability to metastasize to lymph nodes by undergoing the epithelial-mesenchymal transition (EMT), whereby epithelial cells lose their epithelial attributes and acquire a mesenchymal cell phenotype. Metastasis is a leading cause of death for GC patients, and the involved mechanisms are still under investigation. In this review, we summarize the current research on how the inflammatory environment affects GC initiation and metastasis via EMT.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.