ReviewEBioMedicine2020
Paracrine and cell autonomous signalling in pancreatic cancer progression and metastasis.
Review in EBioMedicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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
30 citing papers in PubMed, 42 citations in OpenAlex.
- A CXCR4 targeting peptide delivered by silica nanoparticles eliminates migrating cancer stem cells in pancreatic ductal adenocarcinoma.Scientific reports · 2026Article
- Synergistic Anti-Tumor Efficacy of Modified FOLFIRINOX and NK Cell Therapy in Pancreatic Ductal Adenocarcinoma.Cancers · 2025Article
- Extracellular derived-exosomal micrornas in pancreatic cancer: investigating their diagnostic importance and potential targets for the prevention and treatment in pancreatic cancer.Frontiers in oncology · 2025Review
- Establishment, characterization, and biobanking of 36 pancreatic cancer organoids: prediction of metastasis in resectable pancreatic cancer.Cellular oncology (Dordrecht, Netherlands) · 2024Article
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- Article
- Machine learning identifies SLC6A14 as a novel biomarker promoting the proliferation and metastasis of pancreatic cancer via Wnt/β-catenin signaling.Scientific reports · 2024Article
- Desmoplastic stromal signatures predict patient outcomes in pancreatic ductal adenocarcinoma.Cell reports. Medicine · 2023Article
- Galectin-1 in Pancreatic Ductal Adenocarcinoma: Bridging Tumor Biology, Immune Evasion, and Therapeutic Opportunities.International journal of molecular sciences · 2023Review
- Kupffer cells prevent pancreatic ductal adenocarcinoma metastasis to the liver in mice.Nature communications · 2023Article
- Collective directional migration drives the formation of heteroclonal cancer cell clusters.Molecular oncology · 2023Article
- Tumor Microenvironment in Pancreatic Cancer Pathogenesis and Therapeutic Resistance.Annual review of pathology · 2023Review
- Bioprinted Hydrogels for Fibrosis and Wound Healing: Treatment and Modeling.Gels (Basel, Switzerland) · 2022Review
- Estimating Metastatic Risk of Pancreatic Ductal Adenocarcinoma at Single-Cell Resolution.International journal of molecular sciences · 2022Article
- The Crosstalk between HepG2 and HMC-III Cells: In Vitro Modulation of Gene Expression with Conditioned Media.International journal of molecular sciences · 2022Article
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- Resistance to Gemcitabine in Pancreatic Ductal Adenocarcinoma: A Physiopathologic and Pharmacologic Review.Cancers · 2022Review
- Single-cell analysis of patient-derived PDAC organoids reveals cell state heterogeneity and a conserved developmental hierarchy.Nature communications · 2021Article
- Pancreatic Cancer Small Extracellular Vesicles (Exosomes): A Tale of Short- and Long-Distance Communication.Cancers · 2021Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Pancreatic ductal adenocarcinoma (PDAC) shows remarkable propensity to metastasize. This predilection to escape from the primary tumor is driven by paracrine and autocrine mechanisms that guide cancer cells through a multi-step process concluding with colonization in distant tissues. Although cell-intrinsic features support the metastatic ability of cancer cells, permissive microenvironments within the primary organ and at sites of distant metastasis may be rate-limiting. Identification of cancer cell-extrinsic factors that regulate formation of these environments lend new therapeutic targets for intervening on the metastatic cascade. In addition, the bipolar, yet fundamental, role of the immune system in the metastatic process presents therapeutic opportunities. Herein, we review the current knowledge of the metastatic cascade in PDAC, and propose that genomically stable determinants of metastasis (e.g. the pro-metastatic niche and immune system) are actionable targets for preventing, containing, and treating metastasis in PDAC.
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.