ReviewSeminars in cancer biology2011
The tumor microenvironment in hepatocellular carcinoma: current status and therapeutic targets.
Review in Seminars in cancer biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 217 papers, 3 of them syntheses that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
217 citing papers in PubMed, 3 syntheses or guidelines pooled it, 397 citations in OpenAlex.
- Organoids of liver diseases: From bench to bedside.World journal of gastroenterology · 2019Pooled it
- Matrix metalloproteinase-7 mRNA and protein expression in gastric carcinoma: a meta-analysis.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014Pooled it
- Relationship of serum MMP-7 levels for colorectal cancer: a meta-analysis.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014Pooled it
- Hepatic stellate cells promote structural and functional remodeling of three-dimensional hepatocellular carcinoma coculture spheroids.Molecular biology reports · 2026Article
- Integrated Transcriptomic Analysis Identifies a Putative cfa-miR-10a-Current issues in molecular biology · 2026Article
- Noninvasive Multi-Omics Radiomic Model Integrating scRNA-seq and Bulk RNA-seq for Hepatocellular Carcinoma Prognosis.Journal of imaging informatics in medicine · 2026Article
- Identification of MARCKSL1 as an independent prognostic biomarker and analysis of its potential regulatory network in hepatocellular carcinoma.Discover oncology · 2026Article
- Cytoglobin in Hepatic Stellate Cells Plays Anti-Fibrotic Role in Chronic Liver Injury.Antioxidants (Basel, Switzerland) · 2026Review
- The Molecular Network of Neutrophil Extracellular Traps in Hepatocellular Carcinoma: Biogenesis, Function, and Therapeutic Implications.Molecules (Basel, Switzerland) · 2026Review
- Differential Expression and Distribution of Slco4a1 and Slco1b2 in an Internal Environment Disorder-induced Hepatocellular Carcinoma Mouse Model.Recent patents on anti-cancer drug discovery · 2026Article
- Clinicopathologic and prognostic significance of TIAM2 overexpression in resected hepatocellular carcinoma.Future science OA · 2025Article
- The Immune Microenvironment in Liver Cancer: From Analysis to Targeting.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Coordinated gene expression within sustained STAT3-associated chromatin conformations contributes to hepatocellular carcinoma progression.Cancer communications (London, England) · 2025Article
- Endoplasmic reticulum stress sensor protein PERK in hepatic stellate cells promotes the progression of hepatocellular carcinoma via p38δ MAPK/IL-1β axis.Scientific reports · 2025Article
- Periprosthetic Infection after Endoprosthetic Reconstruction for Femoral Bone Metastases: Incidence and Risk Factors, a Single Center Study.Clinics in orthopedic surgery · 2025Article
- Nanoparticle-based therapeutic strategies for chronic liver diseases: Advances and insights.Liver research (Beijing, China) · 2025Review
- MRI Coregistered Rodent Histotripsy Array for Orthotopic Liver Models.IEEE transactions on ultrasonics, ferroelectrics, and frequency control · 2025Article
- Roles of the gut microbiota in hepatocellular carcinoma: from the gut dysbiosis to the intratumoral microbiota.Cell death discovery · 2025Review
- Overcoming immunotherapy resistance in hepatocellular carcinoma by targeting myeloid IL-8/CXCR2 signaling.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- A novel TLR4 accessory molecule drives hepatic oncogenesis through tumor-associated macrophages.Cancer letters · 2025Article
157 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
A growing body of literature highlights the cross-talk between tumor cells and the surrounding peri-tumoral stroma as a key modulator of the processes of hepatocarcinogenesis, epithelial mesenchymal transition (EMT), tumor invasion and metastasis. The tumor microenvironment can be broadly classified into cellular and non-cellular components. The major cellular components include hepatic stellate cells, fibroblasts, immune, and endothelial cells. These cell types produce the non-cellular components of the tumor stroma, including extracellular matrix (ECM) proteins, proteolytic enzymes, growth factors and inflammatory cytokines. The non-cellular component of the tumor stroma modulates hepatocellular carcinoma (HCC) biology by effects on cancer signaling pathways in tumor cells and on tumor invasion and metastasis. Global gene expression profiling of HCC has revealed that the tumor microenvironment is an important component in the biologic and prognostic classification of HCC. There are substantial efforts underway to develop novel drugs targeting tumor-stromal interactions. In this review, we discuss the current knowledge about the role of the tumor microenvironment in pathogenesis of HCC, the role of the tumor microenvironment in the classification of HCC and efforts to develop treatments targeting the tumor microenvironment.
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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.