ArticleOncogene2013
Cooperation between p53 and the telomere-protecting shelterin component Pot1a in endometrial carcinogenesis.
Article in Oncogene, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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
25 citing papers in PubMed, 37 citations in OpenAlex.
- 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
- Comprehensive analyses of telomerase component DKC1 and its association with clinical, molecular and immune landscapes in uterine corpus endometrial carcinoma.Frontiers in cell and developmental biology · 2025Article
- MYC is Sufficient to Generate Mid-Life High-Grade Serous Ovarian and Uterine Serous Carcinomas in a p53-R270H Mouse Model.Cancer research communications · 2024Article
- MYC is sufficient to generate mid-life high-grade serous ovarian and uterine serous carcinomas in a p53-R270H mouse model.bioRxiv : the preprint server for biology · 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
- A New Type of Endometrial Cancer Models in Mice Revealing the Functional Roles of Genetic Drivers and Exploring their Susceptibilities.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Development of adverse outcome pathways relevant for the identification of substances having endocrine disruption properties Uterine adenocarcinoma as adverse outcome.EFSA journal. European Food Safety Authority · 2023Article
- Heritable defects in telomere and mitotic function selectively predispose to sarcomas.Science (New York, N.Y.) · 2023Article
- Endometrial polyps are non-neoplastic but harbor epithelial mutations in endometrial cancer drivers at low allelic frequencies.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2022Article
- FOXA2 suppresses endometrial carcinogenesis and epithelial-mesenchymal transition by regulating enhancer activity.The Journal of clinical investigation · 2022Article
- Co-existing TP53 and ARID1A mutations promote aggressive endometrial tumorigenesis.PLoS genetics · 2021Article
- Two-Way Development of the Genetic Model for Endometrial Tumorigenesis in Mice: Current and Future Perspectives.Frontiers in genetics · 2021Review
- The enigma of excessively long telomeres in cancer: lessons learned from rare human POT1 variants.Current opinion in genetics & development · 2020Review
- Fbxw7 is a driver of uterine carcinosarcoma by promoting epithelial-mesenchymal transition.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Initiation of Pulmonary Fibrosis after Silica Inhalation in Rats is linked with Dysfunctional Shelterin Complex and DNA Damage Response.Scientific reports · 2019Article
- Telomerase and Telomeres in Endometrial Cancer.Frontiers in oncology · 2019Review
- Modeling Endometrial Cancer: Past, Present, and Future.International journal of molecular sciences · 2018Review
- Telomeres: Implications for Cancer Development.International journal of molecular sciences · 2018Review
- Interleukin-17A Promotes Lung Tumor Progression through Neutrophil Attraction to Tumor Sites and Mediating Resistance to PD-1 Blockade.Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer · 2017Article
- Telomere-driven diseases and telomere-targeting therapies.The Journal of cell biology · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 4 institutions in 1 country.
Funding
Abstract
Type II endometrial cancer (EMCA) represents only 10% of all EMCAs, but accounts for 40% of EMCA-related mortality. Previous studies of human tumors have shown an association between Type II tumors and damaged telomeres. We hypothesized that the lack of murine Type II EMCA models is due to the extremely long telomeres in laboratory mouse strains. We previously showed that telomerase-null mice with critically short telomeres developed endometrial lesions histologically resembling endometrial intraepithelial carcinoma (EIC), the accepted precursor for Type II EMCA. However, these mice did not develop invasive endometrial adenocarcinoma, and instead succumbed prematurely to multi-organ failure. Here, we modeled critical telomere attrition by conditionally inactivating Pot1a, a component of the shelterin complex that stabilizes telomeres, within endometrial epithelium. Inactivation of Pot1a by itself did not stimulate endometrial carcinogenesis, and did not result in detectable DNA damage or apoptosis in endometrium. However, simultaneous inactivation of Pot1a and p53 resulted in EIC-like lesions by 9 months indistinguishable from those seen in late generation telomerase-null mice. These lesions progressed to invasive endometrial adenocarcinomas as early as 9 months of age with metastatic disease in 100% of the animals by 15 months. These tumors were poorly differentiated endometrial adenocarcinomas with prominent nuclear atypia, resembling human Type II cancers. Furthermore, these tumors were aneuploid with double-stranded DNA breaks and end-to-end telomere fusions and most were tetraploid or near-tetraploid. These studies lend further support to the hypothesis that telomeric instability has a critical role in Type II endometrial carcinogenesis and provides an intriguing in-vivo correlate to recent studies implicating telomere-dependent tetraploidization as an important mechanism in carcinogenesis.
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.