ReviewFundamental research2025
Advances in the molecular mechanisms underlying progestin resistance in endometrial cancer.
Review in Fundamental research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
7 citing papers in PubMed.
- Calcium dysregulation in synergy with sonodynamic therapy via medroxyprogesterone-targeted and ROS-responsive nanoparticles for endometrial cancer.Bioactive materials · 2027Article
- Review
- Efficacy of combined metformin plus progestin therapy versus progestin monotherapy in endometrial hyperplasia: a randomized clinical trial.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Sensitive detection of unopposed estrogen using estrogen receptor functionalized nanoprobes for cancer diagnosis.Discover nano · 2026Review
- Progesterone resistance in atypical endometrial hyperplasia: Expression and mechanisms of hormone-responsive molecules.Medicine · 2026Article
- Article
- Canagliflozin alleviates progestin resistance by suppressing RARβ/CRABP2 signaling in THRB knockout endometrial cancer cells.Frontiers in pharmacology · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The incidence of endometrial cancer (EC) has been on the rise, with a notable increase observed in younger female population. Approximately 80% of EC patients are associated with endometrial hyperplasia, a condition characterized by excessive stimulation from unopposed estrogen. Progestin, as the antagonist of estrogen, is recommended for patients with fertility conservation requirements. However, some patients may exhibit insensitivity to progestin treatment, and those with comorbidities such as obesity and diabetes may experience suboptimal therapeutic effects. To improve the efficacy of progestin treatment and address the fertility needs of patients, it is imperative to elucidate the underlying mechanisms of progestin insensitivity in EC. In this review, we explore the role of progestin in EC and its clinical effectiveness. We discuss the factors contributing to progestin insensitivity, highlight recent advancements in research aimed at enhancing treatment sensitivity, and propose potential avenues for future investigation.
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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.