ArticleNature communications2019
Heterogeneity and dynamics of active Kras-induced dysplastic lineages from mouse corpus stomach.
Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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
34 citing papers in PubMed, 64 citations in OpenAlex.
- The origins and progression of pyloric metaplasia following gastric mucosal injury.Physiological reviews · 2026Review
- Managing dangerous liaisons: lessons fromJournal of bacteriology · 2026Review
- Signaling pathways and targeted interventions for precancers.Signal transduction and targeted therapy · 2026Review
- Emerging KRAS G12D inhibitor in the treatment of digestive system tumors: opportunities and challenges.Translational gastroenterology and hepatology · 2026Review
- Epithelial WNT secretion drives niche escape of developing gastric cancer.Molecular cancer · 2025Article
- Listening to the Past, Shaping the Future: A Data-mining Based and Visual Analysis of Five Decades of Gastric Carcinogenesis Research.Biological procedures online · 2025Article
- MR Promotes Ferroptosis in Gastric Cancer by Regulating FANCD2 Expression Mediated by m6A Modification.Applied biochemistry and biotechnology · 2025Article
- Cell Settling, Migration, and Stochastic Cancer Gene Expression Suggest Potassium Membrane Flux May Initiate pH Reversal.Biomolecules · 2025Article
- Advances in modeling gastric intestinal metaplasia: a comprehensive review of experimental models and mechanistic insights.Frontiers in oncology · 2025Review
- Cortactin Facilitates Malignant Transformation of Dysplastic Cells in Gastric Cancer Development.Cellular and molecular gastroenterology and hepatology · 2025Article
- Emerging strategies to investigate the biology of early cancer.Nature reviews. Cancer · 2024Review
- Refining the diagnostic utility of OLFM4 in gastric cancer precursors: a call for rigorous methodologies.Molecular cancer · 2024Article
- Regulation of metaplasia and dysplasia in the stomach by the stromal microenvironment.Experimental & molecular medicine · 2024Review
- Oncogenic Fatty Acid Metabolism Rewires Energy Supply Chain in Gastric Carcinogenesis.Gastroenterology · 2024Article
- Evolution of innate immunity: lessons from mammalian models shaping our current view of insect immunity.Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology · 2024Review
- Spatial Transcriptomics: A Powerful Tool in Disease Understanding and Drug Discovery.Theranostics · 2024Review
- Targeting Stem Cells and Dysplastic Features With Dual MEK/ERK and STAT3 Suppression in Gastric Carcinogenesis.Gastroenterology · 2024Article
- Dynamic tuft cell expansion during gastric metaplasia and dysplasia.The journal of pathology. Clinical research · 2024Article
- Apposition of Fibroblasts With Metaplastic Gastric Cells Promotes Dysplastic Transition.Gastroenterology · 2023Article
- KRAS activation in gastric cancer stem-like cells promotes tumor angiogenesis and metastasis.BMC cancer · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 3 institutions in 2 countries.
Funding
Abstract
Dysplasia is considered a key transition state between pre-cancer and cancer in gastric carcinogenesis. However, the cellular or phenotypic heterogeneity and mechanisms of dysplasia progression have not been elucidated. We have established metaplastic and dysplastic organoid lines, derived from Mist1-Kras(G12D) mouse stomach corpus and studied distinct cellular behaviors and characteristics of metaplastic and dysplastic organoids. We also examined functional roles for Kras activation in dysplasia progression using Selumetinib, a MEK inhibitor, which is a downstream mediator of Kras signaling. Here, we report that dysplastic organoids die or show altered cellular behaviors and diminished aggressive behavior in response to MEK inhibition. However, the organoids surviving after MEK inhibition maintain cellular heterogeneity. Two dysplastic stem cell (DSC) populations are also identified in dysplastic cells, which exhibited different clonogenic potentials. Therefore, Kras activation controls cellular dynamics and progression to dysplasia, and DSCs might contribute to cellular heterogeneity in dysplastic cell lineages.
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.