ArticleWorld journal of hepatology2017
Tumor reactive stroma in cholangiocarcinoma: The fuel behind cancer aggressiveness.
Article in World journal of hepatology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05172310 (PET Imaging of Tumors in Pancreas, Bile Ducts, Stomach and Ovaries by a Novel Tracer, 68Ga-FAPI-46 = Fibroblast Activation Protein Inhibitor), which is not on this map. Cited by 51 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.
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.
PET Imaging of Tumors in Pancreas, Bile Ducts, Stomach and Ovaries by a Novel Tracer, 68Ga-FAPI-46 = Fibroblast Activation Protein Inhibitor
Who cites it
51 citing papers in PubMed, 89 citations in OpenAlex.
- Combined MEK/PD-L1 Inhibition Alters Peripheral Cytokines and Lymphocyte Populations Correlating with Improved Clinical Outcomes in Advanced Biliary Tract Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2022Trial
- A randomized placebo-controlled phase I clinical trial to evaluate the immunomodulatory activities of Atractylodes lancea (Thunb) DC. in healthy Thai subjects.BMC complementary medicine and therapies · 2021Trial
- Fibroblast-associated TPM2 links cell-matrix remodeling to EMT-Notch signaling and gemcitabine resistance in intrahepatic cholangiocarcinoma.Cancer biology & therapy · 2026Article
- SPINK1-driven cellular heterogeneity and interaction networks in intrahepatic cholangiocarcinoma revealed by integrated multi-omics analysis.Journal of advanced research · 2026Article
- Targeting cancer-associated fibroblast-activated HGF/c-MET pathway inhibits extrahepatic cholangiocarcinoma progression and restores gemcitabine therapeutic sensitivity.Acta pharmaceutica Sinica. B · 2026Article
- Therapy-imprinted fibroblast memory in cholangiocarcinoma: rewiring CAF niches for immune evasion and treatment-resistant relapse.Frontiers in immunology · 2026Review
- Molecular mechanisms and genetic features of cholangiocarcinoma: implications for targeted therapeutic strategies.Precision clinical medicine · 2025Review
- Cancer-associated fibroblasts promote growth and dissemination of esophageal squamous cell carcinoma cells by secreting WNT family member 5A.Molecular and cellular biochemistry · 2025Article
- Periductal fibroblasts participate in liver homeostasis, fibrosis, and tumorigenesis.The Journal of experimental medicine · 2025Article
- Hepatic Stellate Cells Functional Heterogeneity in Liver Cancer.Seminars in liver disease · 2025Review
- Cancer-associated fibroblasts in cholangiocarcinoma: the central nexus of tumor-stroma crosstalk and therapeutic translation.Frontiers in immunology · 2025Review
- Stroma-tology: Predicting recurrence in cholangiocarcinoma: Editorial on "Development and validation of a stromal-immune signature to predict prognosis in intrahepatic cholangiocarcinoma".Clinical and molecular hepatology · 2025Article
- Multi-Omics Profiling Unveils the Complexity and Dynamics of Immune Infiltrates in Intrahepatic Cholangiocarcinoma.Biology · 2024Article
- Unveil Intrahepatic Cholangiocarcinoma Heterogeneity through the Lens of Omics and Multi-Omics Approaches.Cancers · 2024Review
- Cordycepin Enhanced Therapeutic Potential of Gemcitabine against Cholangiocarcinoma via Downregulating Cancer Stem-Like Properties.Biomolecules & therapeutics · 2024Article
- THBS1 and THBS2 Enhance the In Vitro Proliferation, Adhesion, Migration and Invasion of Intrahepatic Cholangiocarcinoma Cells.International journal of molecular sciences · 2024Article
- Cancer-Associated Fibroblasts Promote Lymphatic Metastasis in Cholangiocarcinoma via the PDGF-BB/PDGFR-β Mediated Paracrine Signaling Network.Aging and disease · 2024Article
- Cholangiocarcinoma-on-a-chip: A human 3D platform for personalised medicine.JHEP reports : innovation in hepatology · 2024Article
- Single-cell RNA sequencing in cancer research: discovering novel biomarkers and therapeutic targets for immune checkpoint blockade.Cancer cell international · 2023Review
- Cholangiocarcinoma - novel biological insights and therapeutic strategies.Nature reviews. Clinical oncology · 2023Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cholangiocarcinoma (CCA) is a highly aggressive epithelial malignancy still carrying a dismal prognosis, owing to early lymph node metastatic dissemination and striking resistance to conventional chemotherapy. Although mechanisms underpinning CCA progression are still a conundrum, it is now increasingly recognized that the desmoplastic microenvironment developing in conjunction with biliary carcinogenesis, recently renamed tumor reactive stroma (TRS), behaves as a paramount tumor-promoting driver. Indeed, once being recruited, activated and dangerously co-opted by neoplastic cells, the cellular components of the TRS (myofibroblasts, macrophages, endothelial cells and mesenchymal stem cells) continuously rekindle malignancy by secreting a huge variety of soluble factors (cyto/chemokines, growth factors, morphogens and proteinases). Furthermore, these factors are long-term stored within an abnormally remodeled extracellular matrix (ECM), which in turn can deleteriously mold cancer cell behavior. In this review, we will highlight evidence for the active role played by reactive stromal cells (as well as by the TRS-associated ECM) in CCA progression, including an overview of the most relevant TRS-derived signals possibly fueling CCA cell aggressiveness. Hopefully, a deeper knowledge of the paracrine communications reciprocally exchanged between cancer and stromal cells will steer the development of innovative, combinatorial therapies, which can finally hinder the progression of CCA, as well as of other cancer types with abundant TRS, such as pancreatic and breast carcinomas.
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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 OpenQuestion graph.