ArticleThe Journal of clinical investigation2011
Notch1 loss of heterozygosity causes vascular tumors and lethal hemorrhage in mice.
Article in The Journal of clinical investigation, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 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
73 citing papers in PubMed, 119 citations in OpenAlex.
- Multiscale in vivo imaging of tumor evolution using a germline conditional triple-reporter mouse.Nature biotechnology · 2026Article
- AI-driven CRISPR strategies in breast cancer: Organoid modeling, adaptive editing, and precision delivery.Iranian journal of basic medical sciences · 2026Review
- Pulmonary-delivered Anticalin Jagged-1 antagonists reduce experimental airway mucus hyperproduction and obstruction.American journal of physiology. Lung cellular and molecular physiology · 2025Article
- Review
- Tumor microenvironment signaling and therapeutics in cancer progression.Cancer communications (London, England) · 2023Review
- Mutations inProceedings of the National Academy of Sciences of the United States of America · 2022Article
- The developmental origins of Notch-driven intrahepatic bile duct disorders.Disease models & mechanisms · 2021Article
- Comparison of the oncogenomic landscape of canine and feline hemangiosarcoma shows novel parallels with human angiosarcoma.Disease models & mechanisms · 2021Article
- Targeting Notch in oncology: the path forward.Nature reviews. Drug discovery · 2021Review
- Interrogating Cellular Communication in Cancer with Genetically Encoded Imaging Reporters.Radiology. Imaging cancer · 2020Review
- Low doses of ionizing radiation enhance angiogenesis and consequently accelerate post-embryonic development but not regeneration in zebrafish.Scientific reports · 2020Article
- Regulation of Blood and Lymphatic Vessels by Immune Cells in Tumors and Metastasis.Annual review of physiology · 2019Review
- MINAR1 is a Notch2-binding protein that inhibits angiogenesis and breast cancer growth.Journal of molecular cell biology · 2018Article
- Taming the Notch Transcriptional Regulator for Cancer Therapy.Molecules (Basel, Switzerland) · 2018Review
- The Notch Pathway in Breast Cancer Progression.TheScientificWorldJournal · 2018Review
- Uncontrolled angiogenic precursor expansion causes coronary artery anomalies in mice lacking Pofut1.Nature communications · 2017Article
- Vascular heterogeneity and specialization in development and disease.Nature reviews. Molecular cell biology · 2017Review
- Article
- Thyroid Hormone-Induced Activation of Notch Signaling is Required for Adult Intestinal Stem Cell Development During Xenopus Laevis Metamorphosis.Stem cells (Dayton, Ohio) · 2017Article
- Article
13 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
The role of the Notch signaling pathway in tumor development is complex, with Notch1 functioning either as an oncogene or as a tumor suppressor in a context-dependent manner. To further define the role of Notch1 in tumor development, we systematically surveyed for tumor suppressor activity of Notch1 in vivo. We combined the previously described Notch1 intramembrane proteolysis-Cre (Nip1::Cre) allele with a floxed Notch1 allele to create a mouse model for sporadic, low-frequency loss of Notch1 heterozygosity. Through this approach, we determined the cell types most affected by Notch1 loss. We report that the loss of Notch1 caused widespread vascular tumors and organism lethality secondary to massive hemorrhage. These findings reflected a cell-autonomous role for Notch1 in suppressing neoplasia in the vascular system and provide a model by which to explore the mechanism of neoplastic transformation of endothelial cells. Importantly, these results raise concerns regarding the safety of chronic application of drugs targeting the Notch pathway, specifically those targeting Notch1, because of mechanism-based toxicity in the endothelium. Our strategy also can be broadly applied to induce sporadic in vivo loss of heterozygosity of any conditional alleles in progenitors that experience Notch1 activation.
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.