ReviewCancers2018
Extracellular Influences: Molecular Subclasses and the Microenvironment in Pancreatic Cancer.
Review in Cancers, 2018. 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, 50 citations in OpenAlex.
- Desmoplasia and therapeutic resistance in pancreatic ductal adenocarcinoma.Cancer letters · 2026Review
- Review
- Review
- Gene expression dynamics in fibroblasts during early-stage murine pancreatic carcinogenesis.iScience · 2025Article
- Phenotypic heterogeneity and tumor immune microenvironment directed therapeutic strategies in pancreatic ductal adenocarcinoma.Frontiers in immunology · 2025Review
- A bioprinted sea-and-island multicellular model for dissecting human pancreatic tumor-stroma reciprocity and adaptive metabolism.Biomaterials · 2024Article
- Decoding Metabolic Symbiosis between Pancreatic Cancer Cells and Cancer-Associated Fibroblasts Using Cultured Tumor Microenvironment.International journal of molecular sciences · 2023Article
- Cancer-Associated Fibroblasts and Extracellular Matrix: Therapeutical Strategies for Modulating the Cholangiocarcinoma Microenvironment.Current oncology (Toronto, Ont.) · 2023Review
- Mitochondrial Metabolism in Pancreatic Ductal Adenocarcinoma: From Mechanism-Based Perspectives to Therapy.Cancers · 2023Review
- A microfluidic-based PDAC organoid system reveals the impact of hypoxia in response to treatment.Cell death discovery · 2023Article
- Biological and Clinical Impacts of Glucose Metabolism in Pancreatic Ductal Adenocarcinoma.Cancers · 2023Review
- Organoids for Modeling (Colorectal) Cancer in a Dish.Cancers · 2022Review
- Cancer Associated Fibroblast (CAF) Regulation of PDAC Parenchymal (CPC) and CSC Phenotypes Is Modulated by ECM Composition.Cancers · 2022Article
- Paradoxical Behavior of Oncogenes Undermines the Somatic Mutation Theory.Biomolecules · 2022Article
- The role of S100A9 in the interaction between pancreatic ductal adenocarcinoma cells and stromal cells.Cancer immunology, immunotherapy : CII · 2022Article
- Pancreatic Cancer and Cellular Senescence: Tumor Microenvironment under the Spotlight.International journal of molecular sciences · 2021Review
- Review
- TRAIL receptors are expressed in both malignant and stromal cells in pancreatic ductal adenocarcinoma.American journal of cancer research · 2021Article
- Targeting the Stroma in the Management of Pancreatic Cancer.Frontiers in oncology · 2021Review
- 3D Cancer Models: The Need for a Complex Stroma, Compartmentalization and Stiffness.Frontiers in bioengineering and biotechnology · 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
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pancreatic ductal adenocarcinoma (PDAC) is the most prevalent form of pancreatic cancer and carries the worst prognosis of all common cancers. Five-year survival rates have not surpassed 6% for some decades and this lack of improvement in outcome urges a better understanding of the PDAC-specific features which contribute to this poor result. One of the most defining features of PDAC known to contribute to its progression is the abundance of non-tumor cells and material collectively known as the stroma. It is now well recognized that the different non-cancer cell types, signalling molecules, and mechanical properties within a tumor can have both tumor-promoting as well as -inhibitory effects. However, the net effect of this intratumour heterogeneity is not well understood. Heterogeneity in the stromal makeup between patients is even less well established. Such intertumour heterogeneity is likely to be affected by the relative contributions of individual stromal constituents, but how these contributions exactly relate to existing classifications that demarcate intertumour heterogeneity in PDAC is not fully known. In this review, we give an overview of the available evidence by delineating the elements of the PDAC stroma and their contribution to tumour growth. We do so by interpreting the heterogeneity at the gene expression level in PDAC, and how stromal elements contribute to, or interconnect, with this.
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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.