ArticleThe American journal of pathology2011
The mTOR/AKT inhibitor temsirolimus prevents deep infiltrating endometriosis in mice.
Article in The American journal of pathology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 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
47 citing papers in PubMed.
- O-GlcNAc modification regulates autophagy and apoptosis in endometriosis.Functional & integrative genomics · 2026Article
- Targeting angiogenesis in endometriosis: a systematic review and network meta-analysis of VEGF-directed pharmacotherapies.Frontiers in reproductive health · 2025Article
- Progress of ADAM17 in Fibrosis-Related Diseases.Mediators of inflammation · 2025Review
- mTOR inhibitors as potential therapeutics for endometriosis: a narrative review.Molecular human reproduction · 2024Review
- Endometriosis-Associated Ovarian Cancer: From Molecular Pathologies to Clinical Relevance.International journal of molecular sciences · 2024Review
- Molecular Mechanism of Resveratrol and Its Therapeutic Potential on Female Infertility.International journal of molecular sciences · 2024Review
- Digestive system deep infiltrating endometriosis: What do we know.Journal of cellular and molecular medicine · 2023Review
- Endometriosis-Associated Ovarian Carcinomas: How PI3K/AKT/mTOR Pathway Affects Their Pathogenesis.Biomolecules · 2023Review
- Alpinumisoflavone Activates Disruption of Calcium Homeostasis, Mitochondria and Autophagosome to Suppress Development of Endometriosis.Antioxidants (Basel, Switzerland) · 2023Article
- Emerging Drug Targets for Endometriosis.Biomolecules · 2022Review
- The Role of mTOR and eIF Signaling in Benign Endometrial Diseases.International journal of molecular sciences · 2022Review
- Ribosome Biogenesis Serves as a Therapeutic Target for Treating Endometriosis and the Associated Complications.Biomedicines · 2022Article
- Inhibitory Effects of 6,8-Diprenylorobol on Endometriosis Progression in Humans by Disrupting Calcium Homeostasis and Mitochondrial Function.Antioxidants (Basel, Switzerland) · 2022Article
- Serum exosomal miRNA from endometriosis patients correlates with disease severity.Archives of gynecology and obstetrics · 2022Article
- Administration of red ginseng regulates microRNA expression in a mouse model of endometriosis.Clinical and experimental reproductive medicine · 2021Article
- Circulating miRNAs Related to Epithelial-Mesenchymal Transitions (EMT) as the New Molecular Markers in Endometriosis.Current issues in molecular biology · 2021Review
- Can Endometriosis-Related Oxidative Stress Pave the Way for New Treatment Targets?International journal of molecular sciences · 2021Review
- Regulation of Inflammatory and Proliferative Pathways by Fotemustine and Dexamethasone in Endometriosis.International journal of molecular sciences · 2021Article
- The effectiveness of Rutin for prevention of surgical induced endometriosis development in a rat model.Scientific reports · 2021Article
- The cannabinoid receptor CB1 affects the proliferation and apoptosis of adenomyotic human uterine smooth muscle cells of the junctional zone: a mechanism study.Reproductive biology and endocrinology : RB&E · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Deep infiltrating endometriosis (DIE) is a particular clinical and histological entity of endometriosis responsible for chronic pelvic pain and infertility. Here we characterize the proliferative phenotype of DIE cells, to explore the cellular and molecular mechanisms that could explain their aggressive potential. In addition, the inhibition of mTOR/AKT pathway was tested, as a potential treatment of DIE. Included were 22 patients with DIE and 12 control patients without endometriosis. Epithelial and stromal cells were extracted from biopsies of eutopic endometrium and deep infiltrating endometriotic nodules from patients with DIE. Cell proliferation was determined by thymidine incorporation. Oxidative stress was assayed by spectrofluorometry. The ERK and mTOR/AKT pathways were analyzed in vitro by Western blot and for AKT in vivo in a mouse model of DIE. The proliferation rate of eutopic endometrial cells and of deep infiltrating endometriotic cells from DIE patients was higher than that of endometrial cells from controls. The hyperproliferative phenotype of endometriotic cells was associated with an increase in endogenous oxidative stress, and with activation of the ERK and mTOR/AKT pathways. mTOR/AKT inhibition by temsirolimus decreased endometriotic cell proliferation both in vitro and in vivo in a mouse model of DIE. Blocking the mTOR/AKT pathway offers new prospects for the treatment of DIE.
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.