ArticleThe American journal of pathology2015
Activated mutant p110α causes endometrial carcinoma in the setting of biallelic Pten deletion.
Article in The American journal of pathology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 26 citations in OpenAlex.
- Role of INPP4B in the proliferation, migration, invasion, and survival of human endometrial cancer cells.Histology and histopathology · 2024Article
- Single-cell transcriptome profiles the heterogeneity of tumor cells and microenvironments for different pathological endometrial cancer and identifies specific sensitive drugs.Cell death & disease · 2024Article
- Comparison of clinical characteristics and prognosis between type I and type II endometrial cancer: a single-center retrospective study.Discover oncology · 2023Article
- Oncohistones and disrupted development in pediatric-type diffuse high-grade glioma.Cancer metastasis reviews · 2023Review
- ENDOMETRIAL CARCINOMA: THE INTERPLAY OF GENETICS AND HORMONES.Transactions of the American Clinical and Climatological Association · 2023Article
- Review
- Tailored Therapy Based on Molecular Characteristics in Endometrial Cancer.BioMed research international · 2021Review
- Cancer-associated mutations in normal human endometrium: Surprise or expected?Cancer science · 2020Review
- Article
- Clinical actionability of molecular targets in endometrial cancer.Nature reviews. Cancer · 2019Review
- ARID1A and PI3-kinase pathway mutations in the endometrium drive epithelial transdifferentiation and collective invasion.Nature communications · 2019Article
- Ovarian insufficiency and CTNNB1 mutations drive malignant transformation of endometrial hyperplasia with altered PTEN/PI3K activities.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Understanding Obesity as a Risk Factor for Uterine Tumors Using Drosophila.Advances in experimental medicine and biology · 2019Review
- The uterine epithelial loss of Pten is inefficient to induce endometrial cancer with intact stromal Pten.PLoS genetics · 2018Article
- Progression inference for somatic mutations in cancer.Heliyon · 2017Article
- Pancancer modelling predicts the context-specific impact of somatic mutations on transcriptional programs.Nature communications · 2017Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
PTEN and PIK3CA mutations occur with high frequency in uterine endometrioid carcinoma (UEC). Although PTEN mutations are present in complex atypical hyperplasia and carcinoma, PIK3CA mutations are restricted to carcinoma. We generated mouse models harboring Pten loss and/or activated Pik3ca in the endometrial epithelium to investigate their respective roles in the pathogenesis of UEC. Presence of an activated mutant Pik3ca on the background of Pten loss led to aggressive disease, with 100% of mice exhibiting carcinoma. Expression of Pik3ca with E545K mutation alone was unable to cause hyperplasia or cancer in the uterus and did not activate Akt as effectively as Pten deletion in short-term cultures of mouse endometrial epithelium, likely explaining the lack of phenotype in vivo. We also report that nuclear localization of FOXO1 correlated with PTEN mutational status irrespective of the PIK3CA status in endometrial cancer cell lines. Furthermore, gene expression profiles resulting from Pten loss or activation of Pik3ca in primary mouse endometrial epithelial cells exhibit minimal overlap. Thus, Pten and Pik3ca have distinct consequences on the activation of the phosphatidylinositol 3-kinase pathway in endometrial epithelium and are likely to affect other nonoverlapping cellular mechanisms involved in the development and progression of the most common type of uterine cancer.
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