ArticleCancer research2019
Prolactin Promotes Fibrosis and Pancreatic Cancer Progression.
Article in Cancer research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.
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
31 citing papers in PubMed, 1 synthesis or guideline pooled it, 50 citations in OpenAlex.
- Mechanisms of obesity- and diabetes mellitus-related pancreatic carcinogenesis: a comprehensive and systematic review.Signal transduction and targeted therapy · 2023Pooled it
- ORANGE: a machine learning approach for modeling tissue-specific aging from transcriptomic data.Briefings in bioinformatics · 2026Article
- Stress Biology in Cancer: Neuroendocrine-Immune Mechanisms Linking Tumor Progression to Translational Interventions.Cancer communications (London, England) · 2026Review
- Functional remodeling of tissue-resident macrophages leads to distinct immune microenvironment evolution and clinical manifestations in lung adenocarcinoma.Clinical and experimental medicine · 2025Article
- Pulmonary Fibrosis in a Patient With a Prolactinoma on Dopamine Agonists: Coincidence or Consequence.JCEM case reports · 2025Article
- Emerging macrophage-based therapies for cancer: a review of preclinical and clinical advances.Frontiers in immunology · 2025Review
- Impact of tumor type and size on macroscopic tissue core retrieval in endoscopic ultrasound-guided fine needle biopsy for pancreatic malignancies.BMC gastroenterology · 2024Article
- Growth Hormone Receptor Antagonist Markedly Improves Gemcitabine Response in a Mouse Xenograft Model of Human Pancreatic Cancer.International journal of molecular sciences · 2024Article
- Acinar to β-like cell conversion through inhibition of focal adhesion kinase.Nature communications · 2024Article
- Dissecting the immune discrepancies in mouse liver allograft tolerance and heart/kidney allograft rejection.Cell proliferation · 2024Article
- Role of STAT3 in pancreatic cancer.Exploration of targeted anti-tumor therapy · 2024Review
- The Expression of Two Distinct Sets of Glycolytic Enzymes Reveals Differential Effects of Glycolytic Reprogramming on Pancreatic Ductal Tumorigenesis in Mice.Biomedicines · 2023Article
- Fibrosis in Liver and Pancreas: a Review on Pathogenic Significance, Diagnostic Options, and Current Management Strategies.Inflammation · 2023Review
- Pregnancy may have little influence on ground-glass opacities suspected for lung adenocarcinoma.Journal of cancer research and clinical oncology · 2023Article
- Covert actions of growth hormone: fibrosis, cardiovascular diseases and cancer.Nature reviews. Endocrinology · 2022Review
- Focal adhesion kinase-mediated signaling controls the onset of pancreatic cell differentiation.Development (Cambridge, England) · 2022Article
- Stromal architecture directs early dissemination in pancreatic ductal adenocarcinoma.JCI insight · 2022Article
- A diversity outbred F1 mouse model identifies host-intrinsic genetic regulators of response to immune checkpoint inhibitors.Oncoimmunology · 2022Article
- Prolactin: The Third Hormone in Breast Cancer.Frontiers in endocrinology · 2022Review
- Immune Cell Modulation of the Extracellular Matrix Contributes to the Pathogenesis of Pancreatic Cancer.Biomolecules · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 7 institutions in 4 countries.
Funding
Abstract
Pancreatic ductal adenocarcinoma (PDAC) is associated with significant fibrosis. Recent findings have highlighted the profibrotic activity of tissue-resident macrophages in the pancreatic cancer microenvironment. Here, we show that neoplastic pancreatic epithelium, as well as a subset of tissue-resident macrophages, expresses the prolactin-receptor (PRLR). High mobility group box 1-induced prolactin expression in the pancreas maintained FAK1 and STAT3 phosphorylation within the epithelium and stroma. Gain-of-function and loss-of-function experiments demonstrated the essential role of prolactin in promoting collagen deposition and fibrosis. Finally, the signaling cascade downstream of prolactin/PRLR activated STAT3 rather than STAT5 in PDAC. These findings suggest that targeting prolactin together with IL6, a known major activator of STAT3, could represent a novel therapeutic strategy for treating pancreatic cancer. SIGNIFICANCE: Prolactin is a key factor in the cross-talk between the stroma and neoplastic epithelium, functioning to promote fibrosis and PDAC progression.
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.