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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: BACKGROUND, RESULTS. Meshes: Angiopoietin-2, Animals, Biomarkers, Tumor, Carcinoma, Hepatocellular, DNA, Complementary, Disease Models, Animal, Disease Progression, Enzyme-Linked Immunosorbent Assay, Female, Gene Expression Regulation, Neoplastic, Liver Cirrhosis, Liver Neoplasms, Mice, Mice, Inbred C3H, Probability, RNA, Neoplasm, Random Allocation, Reverse Transcriptase Polymerase Chain Reaction, Sensitivity and Specificity, Statistics, Nonparametric, Vascular Endothelial Growth Factor A, Vascular Endothelial Growth Factor Receptor-1.
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Is accelerated orthotopic hepatocellular carcinomas growth linked to increased expression of pro-angiogenic and prometastatic factors in murine liver fibrosis? Context: Most experimental therapy studies are performed in mice that bear subcutaneous or orthotopic hepatoma but are otherwise healthy. We questioned whether a pre-existing fibrosis affects tumour development of implanted syngenic hepatoma cells. To further investigate a selected panel of factors involved in tumour growth, tumour organ samples were characterized for gene expression of vascular endothelial growth factor (VEGF)-A/-C, VEGF receptors Flt1, Flk-1, Flt-4 and for VEGF-A protein levels. The presented data show that tumour sizes were 3.7-fold increased and fibrotic livers had numerous satellites. Increased tumour sizes were associated with elevated intratumoral VEGF-A protein amounts and intratumoral increased VEGF receptor gene expression levels in tumour tissue from fibrotic livers as compared with non-fibrotic livers. Additionally, intratumoral gene expression levels of matrix metalloproteinase-2 (MMP-2) and MMP-9 were elevated in fibrotic mice.
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Our results indicate that liver fibrosis stimulates tumour development of implanted syngenic hepatoma cells. Accelerated tumour growth was going along with elevated intratumoral VEGF-A and VEGF-A receptor status, which most probably mediated pro-angiogenic and prometastatic effects in this model. Furthermore, advanced tumour spread was associated with increased MMP-2/-9 expression. These data suggest that the intratumoral VEGF-A proteins levels and VEGF receptor status contribute to accelerated hepatocellular carcinoma development in fibrotic mice and that elevated MMP-2, MMP-9 and VEGF-C levels could promote tumour metastasis in this model. Final Decision: yes