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Endometriosis from Initiation to Innovation: Immune Microenvironments, Clonal Lesion Biology, and the Emerging Therapeutic Pipeline.

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, …

Published: Sept. 19, 2026, midnight
Integrative mRNA and miRNA Profiling Identifies Shared and Subtype-Associated PI3K-AKT-mTOR Pathway Dysregulation and Candidate miRNA-Mediated Regulatory Interactions in Endometriosis-Associated Ovarian Cancers (EAOCs).

Background: Endometriosis-associated ovarian cancers (EAOCs), including ovarian clear cell (OCCC) and endometrioid ovarian carcinoma (EnOC) subtypes, frequently exhibit transcriptomic dysregulation of the PI3K/AKT/mTOR signalling axis. While genomic aberrations are well-documented, …

Published: Sept. 4, 2026, midnight
Silencing of SEPT9 inhibits proliferation and migration of endometriotic stromal cells via suppression of the PI3K/AKT signaling pathway.

The aim of this study was to investigate the effects of SEPT9 on proliferation, migration, and apoptosis in endometriotic stromal cells and to explore the underlying mechanisms.

Published: Aug. 17, 2026, midnight
Exploring the Possible Role of Endometriosis-Associated Dysbiosis in Endometrial Carcinogenesis.

Background and Objectives: Endometriosis is associated with chronic inflammation, immune dysregulation, oestrogen-dependent growth, oxidative stress, altered steroid hormone metabolism, compromised epithelial barrier integrity, and the production of bioactive microbial metabolites. …

Published: Aug. 17, 2026, midnight
Gut commensal Olsenella profusa promotes endometriosis via lysophosphatidylcholine metabolite.

Endometriosis (EM) is an intractable gynecological condition with uncertain etiology. Gut microbiota have been increasingly implicated in EM, yet the underlying mechanisms remain unclear. Here, we identify a gut microbe-metabolite-uterus …

Published: Aug. 5, 2026, midnight
Steroidal alkaloids as multi-target therapeutics for the treatment of endometriosis.

Endometriosis is a chronic inflammatory disease characterised by ectopic endometrial tissue, progressive fibrosis and chronic pain, with a pathogenesis that goes beyond oestrogen dependence. The central question this review seeks …

Published: July 4, 2026, midnight
Patient-derived organoids in gynaecological cancers: emerging tools for therapy and disease modelling.

Patient-derived organoids (PDOs) have emerged as physiologically relevant three-dimensional (3D) culture systems that closely mimic the molecular and histological features of the human endometrium and associated malignancies. Owing to their …

Published: June 27, 2026, midnight
Inhibiting CSNK2A Suppresses the Viability, Autophagy, Growth and Motility of Ectopic Endometrial Stromal Cells.

Endometriosis is an estrogen-dependent disorder characterized by ectopic growth of endometrial tissue. There is a lack of effective biomarkers for early detection and revealing mechanisms of endometriosis. CSNK2A1 is a …

Published: June 9, 2026, midnight
Anti-NRP1 peptide-engineered ROS/pH dual-responsive nanoparticles for Alpelisib delivery regulate Sema3A-NRP1/PI3K-AKT signaling to balance oxidative stress and inhibit angiogenesis in endometriosis.

Endometriosis progression is driven by oxidative stress and excessive angiogenesis within an inflammatory microenvironment. To overcome these challenges, we designed ROS/pH dual-responsive Alpelisib-loaded nanoparticles (Alp@TAT-AT7-NPs) functionalized with an anti-NRP1 peptide …

Published: June 6, 2026, midnight
Contributions of T-helper 9 cells in endometriosis-associated inflammation and lesion growth.

Endometriosis is an inflammatory gynecologic disease characterized by ectopic growth of endometrial-like tissue, resulting in pelvic pain and infertility. T-helper 9 (Th9) cells play a known role in various chronic …

Published: May 30, 2026, midnight
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