ArticleCancer research2026
Estrogen Production in Pancreatic Cancer Shapes a Tumor-Suppressive Stromal Microenvironment.
Article in Cancer research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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.
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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.
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Who cites it
2 citing papers in PubMed.
- Unveiling the Mysteries of CLEC3B: Physiological Roles, Pathological Impacts, and Research Gaps.Cells · 2026Review
- <p>Unveiling sex differences in pancreatic ductal adenocarcinoma: Current evidence and future directions (Review)</p>.International journal of oncology · 2026Review
Corrections and comments
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Authors and funding
18 authors.
Funding
Abstract
Pancreatic ductal adenocarcinoma (PDAC) is a leading cause of cancer-related death due to a lack of effective therapeutic interventions. PDAC tumors are highly fibrotic, and stromal abundance is hypothesized to contribute to patient outcomes. However, stromal fibroblasts can be tumor promoting and tumor restraining, which could explain the disappointing clinical results of stromal-targeting therapies. In this study, we observed that serum levels of stromal biomarkers associated with favorable outcomes were significantly higher in female patients with PDAC compared with male patients. This was supported by in silico estimates of stromal abundance across solid cancers, as well as magnetic resonance elastography and tissue staining, which revealed that female patients with PDAC had stiffer tumor tissue. Gene expression analysis revealed that estrogen signaling instructs a stromal fibroblast phenotype that is associated with relatively indolent molecular subtypes and a more favorable prognosis, which is maintained by stromal expression of C-type lectin CLEC3B. Remarkably, estrogens were detected intratumorally, and pancreatic cancer cells expressed key enzymes for estrogen synthesis. Estrogen production in PDAC was fueled by the catabolism of stroma-derived branched-chain amino acids, which ultimately resulted in the production of steroid hormone precursors. Together, these data reveal important hormone-driven factors that limit tumor progression by reprogramming the tumor microenvironment and provide leads for therapy development for PDAC. SIGNIFICANCE: Estrogen produced by pancreatic cancer cells alters the phenotype of cancer-associated fibroblasts to shape a tumor-suppressive microenvironment that hampers aggressive disease phenotypes, which could guide the development of stromal-targeted therapies. See related commentary by Veghini and Corbo, p. 567.
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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 Socratic graph.