ArticleBMC medical genomics2025
A lipid metabolism-related gene signature predicts prognosis after tamoxifen treatment in ER + breast cancer and reflects tumor microenvironment heterogeneity through single-cell analysis.
Article in BMC medical genomics, 2025. 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.
- Immune evasion driven by lipid metabolic reprogramming in endocrine-resistant HRFrontiers in immunology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAlthough the clinical outcome of ER + breast cancer patients receiving tamoxifen after surgery is favorable, a proportion of patients experience recurrence or death due to disease progression.
methodsIn this study, by integrating lipid metabolism gene expression and machine learning data, a prognostic model based on gene expression was developed using the TCGA-ER + BRCA dataset (N = 183) and validated with the GSE17705 (N = 298), GSE22219 (N = 134), GSE42568 (N = 70), and GSE58644 (N = 147) datasets. Patients were stratified into high- and low-risk groups based on the median risk score of the signature. Comparative analyses of survival, genomic features, immune infiltration, and drug sensitivity were performed between these groups.
resultsPatients in the high-risk group had worse survival outcomes than those in the low-risk group. The five-year overall survival AUC of the model was 0.858, indicating good performance. High-risk patients were characterized by USH2A and KMT2C mutations, genomic amplification, and enriched JAK-STAT pathway and cytokine-cytokine receptor interaction pathways. Resting CD4 + memory T cells, activated mast cells, and myeloid dendritic cells were significantly enriched in the low-risk group, while M0 macrophages were enriched in the high-risk group. Single-cell sequencing analyses also revealed that the model was significantly associated with macrophages and the percentage of proliferating myeloid cells. The signature was also associated with sensitivity to multiple drugs. Cell-cell interaction difference analyses suggested that cancer-related signaling pathways, especially the SIRPα/CD47/IL6 pathway, were decreased in high-risk patients, but these samples exhibited increased SPP1 interactions.
conclusionThe signature captures lipid metabolic reprogramming and immunosuppression, providing a biomarker for prognosis and precision therapy in tamoxifen-treated ER + breast cancer.
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.