ArticleCommunications biology2026
Dynamic uterine microenvironment drives endometrial adenocarcinoma carcinogenesis and progression.
Article in Communications biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
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
Endometrial cancer (EC) development is driven by the interaction between the tumor and the microenvironment. However, the immune microenvironment dynamics during this process are not clear. Here, we applied single-cell RNA sequencing (scRNA-seq) to uterine blood samples collected at hysterectomy from 15 individuals encompassing four groups-benign controls, endometrial intraepithelial neoplasia (EIN), the transition from EIN to carcinoma, and EC. Uterine blood, obtained without prior enrichment, provides a liquid biopsy of the local tumor milieu, enabling high-resolution profiling of both immune and stromal cells in a minimally invasive manner. Our analysis revealed simultaneous immune and stromal remodeling in early premalignant lesions. Notably, even in EIN, we observed significant immune cell reprogramming alongside the emergence of protumorigenic stromal-epithelial interactions. Importantly, we discovered predictive single-cell transcriptomic signatures derived from neutrophils that stratify patients according to disease state, highlighting the potential of tumor-educated innate immune cells as biomarkers. These findings yield candidate cellular and molecular signatures, particularly from neutrophils, that could enhance early EC detection and guide therapeutic strategies. Our work provides a proof-of-concept for leveraging local liquid biopsies in single-cell oncology, offering new insights into EC initiation and development, paving the way for noninvasive diagnostics on the basis of single-cell transcriptomic profiles.
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.