ArticleThe American journal of pathology2013
Type I to type II ovarian carcinoma progression: mutant Trp53 or Pik3ca confers a more aggressive tumor phenotype in a mouse model of ovarian cancer.
Article in The American journal of pathology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 55 citations in OpenAlex.
- A combined biomarker panel shows improved sensitivity for the early detection of ovarian cancer allowing the identification of the most aggressive type II tumours.British journal of cancer · 2017Trial
- The Interdependence of Carbon Substrates and Metabolic Pathways Enables the Metabolic Plasticity of Cancer Cells.Advances in experimental medicine and biology · 2026Review
- Ovarian Cancer-Epidemiology, Classification, Pathogenesis, Treatment, and Estrogen Receptors' Molecular Backgrounds.International journal of molecular sciences · 2025Review
- Role of Akt/Protein Kinase B in Cancer Metastasis.Biomedicines · 2023Review
- Replication stress and defective checkpoints make fallopian tube epithelial cells putative drivers of high-grade serous ovarian cancer.Cell reports · 2023Article
- Establishment of a novel model of endometriosis-associated ovarian cancer by transplanting uterine tissue from Arid1a/Pten knockout mice.Scientific reports · 2023Article
- PIK3CA gene aberrancy and role in targeted therapy of solid malignancies.Cancer gene therapy · 2020Review
- MicroRNA-200 family governs ovarian inclusion cyst formation and mode of ovarian cancer spread.Oncogene · 2020Article
- Validation of Novel Prognostic Biomarkers for Early-Stage Clear-Cell, Endometrioid and Mucinous Ovarian Carcinomas Using Immunohistochemistry.Frontiers in oncology · 2020Article
- Metabolic Remodeling as a Way of Adapting to Tumor Microenvironment (TME), a Job of Several Holders.Advances in experimental medicine and biology · 2020Review
- Trp53 null and R270H mutant alleles have comparable effects in regulating invasion, metastasis, and gene expression in mouse colon tumorigenesis.Laboratory investigation; a journal of technical methods and pathology · 2019Article
- Challenges for the Clinical Development of PI3K Inhibitors: Strategies to Improve Their Impact in Solid Tumors.Cancer discovery · 2019Review
- Review
- Glutathione in Ovarian Cancer: A Double-Edged Sword.International journal of molecular sciences · 2018Review
- Protein expression patterns in cancer-associated fibroblasts and cells undergoing the epithelial-mesenchymal transition in ovarian cancers.Oncotarget · 2018Article
- When Is "Type I" Ovarian Cancer Not "Type I"? Indications of an Out-Dated Dichotomy.Frontiers in oncology · 2018Review
- The Functions of MicroRNA-200 Family in Ovarian Cancer: Beyond Epithelial-Mesenchymal Transition.International journal of molecular sciences · 2017Review
- Emerging diagnostic, prognostic and therapeutic biomarkers for ovarian cancer.Cellular oncology (Dordrecht, Netherlands) · 2017Review
- Article
- Recent Advances in Understanding, Diagnosing, and Treating Ovarian Cancer.F1000Research · 2017Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
A dualistic pathway model of ovarian carcinoma (OvCA) pathogenesis has been proposed: type I OvCAs are low grade, genetically stable, and relatively more indolent than type II OvCAs, most of which are high-grade serous carcinomas. Endometrioid OvCA (EOC) is a prototypical type I tumor, often harboring mutations that affect the Wnt and phosphatidylinositol 3-kinase/AKT/mammalian target of rapamycin signaling pathways. Molecular and histopathologic analyses indicate type I and II OvCAs share overlapping features, and a subset of EOCs may undergo type I→type II progression accompanied by acquisition of somatic TP53 or PIK3CA mutations. We used a murine model of EOC initiated by conditional inactivation of the Apc and Pten tumor suppressor genes to investigate mutant Trp53 or Pik3ca alleles as key drivers of type I→type II OvCA progression. In the mouse EOC model, the presence of somatic Trp53 or Pik3ca mutations resulted in shortened survival and more widespread metastasis. Activation of mutant Pik3ca alone had no demonstrable effect on the ovarian surface epithelium but resulted in papillary hyperplasia when coupled with Pten inactivation. Our findings indicate that the adverse prognosis associated with TP53 and PIK3CA mutations in human cancers can be functionally replicated in mouse models of type I→type II OvCA progression. Moreover, the models should represent a robust platform for assessment of the contributions of Trp53 or Pik3ca defects in the response of EOCs to conventional and targeted drugs.
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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.