ReviewCancer letters2026
Endometriosis from initiation to innovation: Immune microenvironments, clonal lesion biology, and the emerging therapeutic pipeline.
Review in Cancer letters, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
Abstract
Endometriosis is a chronic, estrogen-dependent inflammatory disease that, despite its benign histology, displays several cancer-relevant features, including clonal expansion, somatic alteration-associated lesion evolution, tissue invasion, apoptosis resistance, immune evasion, angiogenesis, fibrosis, and metabolic adaptation. These features are particularly important in ovarian endometriosis, where recurrent hemorrhage, iron-driven oxidative stress, and chronic inflammatory remodeling may promote malignant transformation. This review examines endometriosis through an oncologic framework by integrating current evidence on disease initiation, clonal lesion evolution, and the peritoneal, ovarian, and deep-infiltrating microenvironments. We discuss how epithelial, stromal, immune, endothelial, mesothelial, and neural components cooperate to support lesion survival, dissemination, vascularization, fibrosis, neuroinflammation, and treatment resistance. Particular attention is given to cancer-associated molecular programs, including PI3K-AKT-mTOR, RAS-MAPK, WNT/β-catenin, hypoxia, oxidative-stress, inflammatory, and epigenetic signaling, and their relationship to endometriosis-associated ovarian cancer. We also critically evaluate animal models, organoids, three-dimensional scaffolds, and microfluidic systems for their ability to reproduce lesion heterogeneity, microenvironmental interactions, therapeutic responses, and malignant progression. Finally, we assess current and emerging therapeutic strategies, emphasizing non-hormonal interventions directed against inflammatory, immune, fibrotic, angiogenic, metabolic, and oncogenic vulnerabilities, together with biomarker-guided and fertility-sparing approaches. Viewing endometriosis as a cancer-relevant inflammatory and clonal disease may reveal actionable mechanisms for precision treatment and interception of endometriosis-associated malignancy.
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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.