ArticleMolecular endocrinology (Baltimore, Md.)2014
Tumor repressor protein 53 and steroid hormones provide a new paradigm for ovarian cancer metastases.
Article in Molecular endocrinology (Baltimore, Md.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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
11 citing papers in PubMed, 14 citations in OpenAlex.
- Polyploid giant cancer cells and ovarian cancer: new insights into mitotic regulators and polyploidy†.Biology of reproduction · 2021Review
- WOMEN IN REPRODUCTIVE SCIENCE: Discovering science and the ovary: a career of joy.Reproduction (Cambridge, England) · 2019Review
- GREB1 is an estrogen receptor-regulated tumour promoter that is frequently expressed in ovarian cancer.Oncogene · 2018Article
- Lifestyle and Reproductive Factors and Ovarian Cancer Risk by p53 and MAPK Expression.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2018Article
- Mutant p53 Promotes Epithelial Ovarian Cancer by Regulating Tumor Differentiation, Metastasis, and Responsiveness to Steroid Hormones.Cancer research · 2016Article
- Deletion of Arid1a in Reproductive Tract Mesenchymal Cells Reduces Fertility in Female Mice.Biology of reproduction · 2016Article
- The role of peptidylarginine deiminase 4 in ovarian cancer cell tumorigenesis and invasion.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- Specific TP53 Mutants Overrepresented in Ovarian Cancer Impact CNV, TP53 Activity, Responses to Nutlin-3a, and Cell Survival.Neoplasia (New York, N.Y.) · 2015Article
- FOXO1/3 and PTEN Depletion in Granulosa Cells Promotes Ovarian Granulosa Cell Tumor Development.Molecular endocrinology (Baltimore, Md.) · 2015Article
- Global deletion of Trp53 reverts ovarian tumor phenotype of the germ cell-deficient white spotting variant (Wv) mice.Neoplasia (New York, N.Y.) · 2015Article
- Iodine-125 induces apoptosis via regulating p53, microvessel density, and vascular endothelial growth factor in colorectal cancer.World journal of surgical oncology · 2014Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
The functional status of the tumor repressor protein (TP53 or TRP53) is a defining feature of ovarian cancer. Mutant or null alleles of TP53 are expressed in greater than 90% of all high-grade serous adenocarcinomas. Wild-type TP53 is elevated in low-grade serous adenocarcinomas in women and in our Pten;Kras;Amhr2-Cre mutant mouse model. Disruption of the Trp53 gene in this mouse model did not lead to high-grade ovarian cancer but did increase expression of estrogen receptor α (ESR1) and markedly enhanced the responsiveness of these cells to estrogen. Specifically, when Trp53-positive and Trp53 null mutant mice were treated with estradiol or vehicle, only the Trp53 null and Esr1-positive tumors respond vigorously to estradiol in vivo and exhibit features characteristic of high-grade type ovarian cancer: invasive growth into the ovarian stroma, rampant metastases to the peritoneal cavity, and nuclear atypia. Estrogen promoted and progesterone suppressed the growth of Trp53 null ovarian tumors and tumor cells injected ip, sc, or when grown in matrigel. Exposure of the Trp53 depleted cells to estrogen also has a profound impact on the tumor microenvironment and immune-related events. These results led to the new paradigm that TRP53 status is related to the susceptibility of transformed ovarian surface epithelial cells to estradiol-induced metastases and nuclear atypia via increased levels of estradiol receptor α.
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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.