ArticleNature genetics2020
Early TP53 alterations engage environmental exposures to promote gastric premalignancy in an integrative mouse model.
Article in Nature genetics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
49 citing papers in PubMed, 1 synthesis or guideline pooled it, 64 citations in OpenAlex.
- Targeting p53 pathways: mechanisms, structures, and advances in therapy.Signal transduction and targeted therapy · 2023Pooled it
- Targeting the YAP-BST2 Axis Overcomes Intrinsic Anti-PD-1 Resistance in Metastatic Gastric Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Reframing early gastric carcinogenesis through lineage, niche, and evolution.Cancer metastasis reviews · 2026Review
- Esophageal cancer: from pathogenesis to precision therapies.Signal transduction and targeted therapy · 2026Review
- Construction and application of a genetically engineered mouse model of gastric adenocarcinoma.Journal of the Chinese Medical Association : JCMA · 2026Article
- 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
- Advances in the study of the relationship between neurotransmitters and gastric cancer.World journal of gastroenterology · 2025Review
- Research advancements and evaluation of multifactor-induced murine models for gastric cancer.Animal models and experimental medicine · 2025Review
- Targetable pathways for drug repurposing in gastric cancer.World journal of gastroenterology · 2025Review
- Yunweiling alleviates functional constipation: integrating network pharmacology and experimental study.Animal models and experimental medicine · 2025Article
- PCMR: a comprehensive precancerous molecular resource.Scientific data · 2025Article
- Article
- Emerging strategies to investigate the biology of early cancer.Nature reviews. Cancer · 2024Review
- Hippo cooperates with p53 to regulate lung airway mucous cell metaplasia.Disease models & mechanisms · 2024Article
- Molecular evolution of intestinal-type early gastric cancer according to Correa cascade.Journal of biomedical research · 2024Article
- Origins of cancer: ain't it just mature cells misbehaving?The EMBO journal · 2024Review
- Modeling human gastric cancers in immunocompetent mice.Cancer biology & medicine · 2024Review
- Tumor initiation and early tumorigenesis: molecular mechanisms and interventional targets.Signal transduction and targeted therapy · 2024Review
- Understanding the complexity of p53 in a new era of tumor suppression.Cancer cell · 2024Review
- Exploring the therapeutic mechanisms of Coptidis Rhizoma in gastric precancerous lesions: a network pharmacology approach.Discover oncology · 2024Article
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17 authors at 5 institutions in 1 country.
Funding
Abstract
Somatic alterations in cancer genes are being detected in normal and premalignant tissue, thus placing greater emphasis on gene-environment interactions that enable disease phenotypes. By combining early genetic alterations with disease-relevant exposures, we developed an integrative mouse model to study gastric premalignancy. Deletion of Trp53 in gastric cells confers a selective advantage and promotes the development of dysplasia in the setting of dietary carcinogens. Organoid derivation from dysplastic lesions facilitated genomic, transcriptional and functional evaluation of gastric premalignancy. Cell cycle regulators, most notably Cdkn2a, were upregulated by p53 inactivation in gastric premalignancy, serving as a barrier to disease progression. Co-deletion of Cdkn2a and Trp53 in dysplastic gastric organoids promoted cancer phenotypes but also induced replication stress, exposing a susceptibility to DNA damage response inhibitors. These findings demonstrate the utility of mouse models that integrate genomic alterations with relevant exposures and highlight the importance of gene-environment interactions in shaping the premalignant state.
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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.