ReviewCells2024
Effects of Angiogenic Factors on the Epithelial-to-Mesenchymal Transition and Their Impact on the Onset and Progression of Oral Squamous Cell Carcinoma: An Overview.
Review in Cells, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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
15 citing papers in PubMed.
- Cancer-Associated Fibroblast-Derived FGF7 Promotes Immune Escape in Oral Squamous Cell Carcinoma via JAK/STAT3-Mediated PD-L1 Expression.Molecular carcinogenesis · 2026Article
- CYP4B1 inhibits lung adenocarcinoma metastasis by downregulating slug transcription via Sp1.Clinical & experimental metastasis · 2026Article
- Tissue engineering driven regeneration in oral squamous cell carcinoma: from biomaterials to precision gene editing.Journal of the Egyptian National Cancer Institute · 2026Review
- Pharmacological Targeting of Angiogenesis in Head and Neck Cancer: Molecular Mechanisms and Emerging Therapeutic Strategies.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Carcinogenic Medications: A Review of Specific Agents and Molecular Mechanisms of Carcinogenesis.Cancer reports (Hoboken, N.J.) · 2026Review
- Partial-EMT in oral squamous cell carcinoma: molecular circuitry and clinical translation.International journal of oral science · 2026Review
- Fibronectin Is a Likely Therapeutic Target Shared by Oral and Breast Carcinomas.International journal of molecular sciences · 2026Article
- Prediction of loss of heterozygosity in oral cavity dysplasia through vascular pattern.Frontiers in oral health · 2026Article
- The Anti-EMMPRIN Monoclonal Antibody hMR18-mAb Induces Tumor Dormancy and Inhibits the EMT Process in Human Carcinoma Cell Lines Co-Cultured with Macrophages.Biomedicines · 2025Article
- Targeted Therapies in Oral and Oropharyngeal Cancer: An Overview of Emerging and Repurposed Agents.Cancers · 2025Review
- miR-107 modulates EMT progression of OSCC by targeting SNCG and inhibiting the ERK/NF-κB signaling pathways.Journal of translational medicine · 2025Article
- Immune Evasion in Head and Neck Squamous Cell Carcinoma: Roles of Cancer-Associated Fibroblasts, Immune Checkpoints, andCancers · 2025Review
- Article
- Delivery of an ERK inhibitor using bioactive lipid nanoparticles reduces angiogenesis and prevents oral squamous cell carcinoma development.Journal of nanobiotechnology · 2025Article
- Exosomes in oral squamous cell carcinoma: functions, challenges, and potential applications.Frontiers in oncology · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
High levels of vascular endothelial growth factor (VEGF), fibroblast growth factor (FGF)-2 and angiopoietin (ANG)-2 are found in tissues from oral squamous cell carcinoma (OSCC) and oral potentially malignant disorders (OPMDs). As might be expected, VEGF, FGF-2, and ANG-2 overexpression parallels the development of new blood and lymphatic vessels that nourish the growing OPMDs or OSCCs and provide the latter with metastatic routes. Notably, VEGF, FGF-2, and ANG-2 are also linked to the epithelial-to-mesenchymal transition (EMT), a trans-differentiation process that respectively promotes or exasperates the invasiveness of normal and neoplastic oral epithelial cells. Here, we have summarized published work regarding the impact that the interplay among VEGF, FGF-2, ANG-2, vessel generation, and EMT has on oral carcinogenesis. Results from the reviewed studies indicate that VEGF, FGF-2, and ANG-2 spark either protein kinase B (AKT) or mitogen-activated protein kinases (MAPK), two signaling pathways that can promote both EMT and new vessels' formation in OPMDs and OSCCs. Since EMT and vessel generation are key to the onset and progression of OSCC, as well as to its radio- and chemo-resistance, these data encourage including AKT or MAPK inhibitors and/or antiangiogenic drugs in the treatment of this malignancy.
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.