ArticleMolecular cancer research : MCR2019
RETRACTED: KRAS Activation in Gastric Adenocarcinoma Stimulates Epithelial-to-Mesenchymal Transition to Cancer Stem-Like Cells and Promotes Metastasis.
Article in Molecular cancer research : MCR, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 30 papers, 1 of them a synthesis that pooled it.
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
30 citing papers in PubMed, 1 synthesis or guideline pooled it, 54 citations in OpenAlex.
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- Oxaliplatin and 5-fluorouracil promote epithelial-mesenchymal transition via activation of KRAS/ERK/NF-κB pathway in KRAS-mutated colon cancer cells.Molecular and cellular biochemistry · 2025Article
- More powerful dysregulation of Helicobacter pylori East Asian-type CagA on intracellular signalings.BMC microbiology · 2024Article
- Retraction: Role of Rac1 Pathway in Epithelial-to-Mesenchymal Transition and Cancer Stem-like Cell Phenotypes in Gastric Adenocarcinoma.Molecular cancer research : MCR · 2024Article
- Retraction: KRAS Activation in Gastric Adenocarcinoma Stimulates Epithelial-to-Mesenchymal Transition to Cancer Stem-Like Cells and Promotes Metastasis.Molecular cancer research : MCR · 2024Article
- Modeling human gastric cancers in immunocompetent mice.Cancer biology & medicine · 2024Review
- The potential contribution of aberrant cathepsin K expression to gastric cancer pathogenesis.Discover oncology · 2024Article
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- Peristalsis-Associated Mechanotransduction Drives Malignant Progression of Colorectal Cancer.Cellular and molecular bioengineering · 2023Article
- KRAS activation in gastric cancer stem-like cells promotes tumor angiogenesis and metastasis.BMC cancer · 2023Article
- System Analysis Based on Lipid-Metabolism-Related Genes Identifies AGT as a Novel Therapy Target for Gastric Cancer with Neoadjuvant Chemotherapy.Pharmaceutics · 2023Article
- Patient-derived spheroids and patient-derived organoids simulate evolutions of lung cancer.Heliyon · 2023Article
- Association between INDELs in MicroRNAs and Susceptibility to Gastric Cancer in Amazonian Population.Genes · 2022Article
- Impacts and mechanisms of metabolic reprogramming of tumor microenvironment for immunotherapy in gastric cancer.Cell death & disease · 2022Review
- Dynamic Changes in Myofibroblasts Affect the Carcinogenesis and Prognosis of Bladder Cancer Associated With Tumor Microenvironment Remodeling.Frontiers in cell and developmental biology · 2022Article
- The origin of gastric cancer stem cells and their effects on gastric cancer: Novel therapeutic targets for gastric cancer.Frontiers in oncology · 2022Review
Corrections and comments
- Retraction · 2024-11-01Concerns/Issues about Image · Duplication of/in Image · Investigation by Journal/Publisher ·
- Retracted
Authors and funding
8 authors at 4 institutions in 3 countries.
Funding
Abstract
Our previous work showed that in a mouse model of gastric adenocarcinoma with loss of
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.