ArticleCancer research2011
Stromal deletion of the APC tumor suppressor in mice triggers development of endometrial cancer.
Article in Cancer research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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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
37 citing papers in PubMed, 59 citations in OpenAlex.
- APC loss promotes endometrial cancer progression by upregulating FGF12 expression: An integrated multi-omics analysis.Chinese medical journal · 2026Article
- Does immunotherapy hold great promise in endometrial cancer care?Frontiers in immunology · 2026Review
- Advances in the molecular mechanisms underlying progestin resistance in endometrial cancer.Fundamental research · 2025Review
- Roles of estrogen receptor α in endometrial carcinoma (Review).Oncology letters · 2023Review
- Endometrial hyperplasia with loss of APC in a novel population of Lyz2-expressing mouse endometrial epithelial cells.Carcinogenesis · 2023Article
- Exosomal miR-125b-5p derived from cancer-associated fibroblasts promotes the growth, migration, and invasion of pancreatic cancer cells by decreasing adenomatous polyposis coli (APC) expression.Journal of gastrointestinal oncology · 2023Article
- To Identify Adenomatous Polyposis Coli Gene Mutation as a Predictive Marker of Endometrial Cancer Immunotherapy.Frontiers in cell and developmental biology · 2022Article
- Endometrial cancer.Nature reviews. Disease primers · 2021Review
- Wnt-Independent and Wnt-Dependent Effects of APC Loss on the Chemotherapeutic Response.International journal of molecular sciences · 2020Review
- 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
- Review
- Targeting the tumour stroma to improve cancer therapy.Nature reviews. Clinical oncology · 2018Review
- Inhibition of extracellular matrix mediated TGF-β signalling suppresses endometrial cancer metastasis.Oncotarget · 2017Article
- Specific deletion of LKB1/Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Article
- Ovarian hormones through Wnt signalling regulate the growth of human and mouse ovarian cancer initiating lesions.Oncotarget · 2016Article
- Stromal Clues in Endometrial Carcinoma: Loss of Expression of β-Catenin, Epithelial-Mesenchymal Transition Regulators, and Estrogen-Progesterone Receptor.International journal of gynecological pathology : official journal of the International Society of Gynecological Pathologists · 2016Article
- Influence of Cancer-Associated Endometrial Stromal Cells on Hormone-Driven Endometrial Tumor Growth.Hormones & cancer · 2015Article
- Genetic instability in the tumor microenvironment: a new look at an old neighbor.Molecular cancer · 2015Review
- The ovary is an alternative site of origin for high-grade serous ovarian cancer in mice.Endocrinology · 2015Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
The contribution of the stromal microenvironment to the progression of endometrial cancer has not been well explored. We have conditionally expressed a mutant allele of adenomatous polyposis coli (APC(cKO)) in murine uterine stroma cells to study its effect on uterine development and function. In addition to metrorrhagia, the mice develop complex atypical endometrial gland hyperplasia that progresses to endometrial carcinoma in situ and endometrial adenocarcinoma as evidenced by myometrial invasion. Stromal cells subjacent to the carcinoma cells express alpha-smooth muscle actin (αSMA) with fewer cells expressing platelet-derived growth factor α compared with normal stromal cells, suggesting that the mutant stromal cells have acquired a more myofibroblastic phenotype, which have been described as cancer-associated fibroblasts and have been shown to induce carcinogenesis in other organ systems. Analyses of human endometrial cancer specimens showed substantial αSMA expression in the stroma compared with normal endometrial stroma cells. We also show that APC(cKO) mutant uteri and human endometrial cancer have decreased stromal levels of transforming growth factor β and bone morphogenetic protein activities and that the mutant uteri failed to respond to exogenous estradiol stimulation. The mutant stroma cells also had higher levels of vascular endothelial growth factor and stromal derived factor signaling components and diminished expression of estrogen receptor α and progesterone receptor, which is common in advanced stages of human endometrial cancer and is an indicator of poor prognosis. Our results indicate that de novo mutation or loss of heterozygosity in stromal APC is sufficient to induce endometrial hyperplasia and endometrial carcinogenesis by mechanisms that are consistent with unopposed estrogen signaling in the endometrial epithelium.
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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.