ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2023
In Vivo Intra-Uterine Delivery of TAT-Fused Cre Recombinase and CRISPR/Cas9 Editing System in Mice Unveil Histopathology of Pten/p53-Deficient Endometrial Cancers.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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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.
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Who cites it
16 citing papers in PubMed, 12 citations in OpenAlex.
- Targeted Nanoparticle Delivery CRISPR/Cas9: overcoming biological barriers, enhancing stability, and improving therapeutic precision.International journal of pharmaceutics: X · 2026Review
- Engineered bacteria as exogenous organelle mimics restore PTEN and p53 tumor suppressor functions for cancer therapy.Nature communications · 2026Article
- Shengxian decoction suppresses malignant progression of lung adenocarcinoma by enhancing CD8Chinese medicine · 2026Article
- Delivery Systems for Therapeutic Genome Editing: Challenges, Innovations, and Future Perspectives.MedComm · 2026Review
- Expression of purinergic receptor P2Y, G-protein coupled 2, is regulated by estrogen during the estrous cycle in mouse uterus.Purinergic signalling · 2026Article
- Application of nanoparticles in the therapeutic management of endometrial cancer.European journal of medical research · 2026Review
- Multiplexed CRISPR/Cas9 Editing of Tumor Suppressor Genes in the Mouse Endometrium Recapitulates High-Risk Endometrial Carcinoma.Cancer communications (London, England) · 2026Article
- Endometrial cancer progression driven by PTEN-deficiency requires miR-424(322)Cell death & disease · 2025Article
- Unlocking the Secrets of the Endometrium: Stem Cells, Niches and Modern Methodologies.Biomedicines · 2025Review
- Genome Editing in Gynecological Oncology: The Emerging Role of CRISPR/Cas9 in Precision Cancer Therapy.Therapeutic innovation & regulatory science · 2025Review
- The Diverse Aspects of Uterine Serous Cancer: an NCI workshop on the status of and opportunities for advancement of research.Journal of the National Cancer Institute · 2025Article
- FBXW7 Directly Ubiquitinates and Degrades CTNNB1 Mediating the Suppression of ENKUR in Endometrial Cancer.International journal of biological sciences · 2025Article
- Oxidative stress-mediated PANoptosis and ferroptosis: Exploration of multimodal cell death triggered by an AIE-active nano-photosensitizer via photodynamic therapy.Theranostics · 2025Article
- Bioengineering approaches for the endometrial research and application.Materials today. Bio · 2024Review
- Construction and Evaluation of BAL-PTX Co-Loaded Lipid Nanosystem for Promoting the Anti-Lung Cancer Efficacy of Paclitaxel and Reducing the Toxicity of Chemotherapeutic Drugs.International journal of nanomedicine · 2024Article
- In Vivo Intra-Uterine Delivery of TAT-Fused Cre Recombinase and CRISPR/Cas9 Editing System in Mice Unveil Histopathology of Pten/p53-Deficient Endometrial Cancers.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
Phosphatase and TENsin homolog (Pten) and p53 are two of the most frequently mutated tumor suppressor genes in endometrial cancer. However, the functional consequences and histopathological manifestation of concomitant p53 and Pten loss of function alterations in the development of endometrial cancer is still controversial. Here, it is demonstrated that simultaneous Pten and p53 deletion is sufficient to cause epithelial to mesenchymal transition phenotype in endometrial organoids. By a novel intravaginal delivery method using HIV1 trans-activator of transcription cell penetrating peptide fused with a Cre recombinase protein (TAT-Cre), local ablation of both p53 and Pten is achieved specifically in the uterus. These mice developed high-grade endometrial carcinomas and a high percentage of uterine carcinosarcomas resembling those found in humans. To further demonstrate that carcinosarcomas arise from epithelium, double Pten/p53 deficient epithelial cells are mixed with wild type stromal and myometrial cells and subcutaneously transplanted to Scid mice. All xenotransplants resulted in the development of uterine carcinosarcomas displaying high nuclear pleomorphism and metastatic potential. Accordingly, in vivo CRISPR/Cas9 disruption of Pten and p53 also triggered the development of metastatic carcinosarcomas. The results unfadingly demonstrate that simultaneous deletion of p53 and Pten in endometrial epithelial cells is enough to trigger epithelial to mesenchymal transition that is consistently translated to the formation of uterine carcinosarcomas in vivo.
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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.