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Updated: Dec 29, 2025
A Preclinical Murine Model of Hepatic Metastases
Published on: September 27, 2014
Preclinical murine tumor models: a structural and functional perspective
Marion V Guerin1, Veronica Finisguerra2, Benoit J Van den Eynde2
1Université de Paris, Institut Cochin, INSERM, U1016, CNRS, UMR8104, F-75014, Paris, France.
Abstract:
The goal of this review is to pinpoint the specific features, including the weaknesses, of various tumor models, and to discuss the reasons why treatments that are efficient in murine tumor models often do not work in clinics. In a detailed comparison of transplanted and spontaneous tumor models, we focus on structure-function relationships in the tumor microenvironment. For instance, the architecture of the vascular tree, which depends on whether tumor cells have gone through epithelial-mesenchymal transition, is determinant for the extension of the spontaneous necrosis, and for the intratumoral localization of the immune infiltrate. Another key point is the model-dependent abundance of TGFβ in the tumor, which controls the variable susceptibility of different tumor models to treatments. Grounded in a historical perspective, this review provides a rationale for checking factors that will be key for the transition between preclinical murine models and clinical applications.
Insights
This review compares murine tumor models, highlighting their weaknesses and why cancer treatments fail in clinics. Understanding tumor microenvironment factors is key for translating preclinical findings to human applications.
Area of Science:
- Oncology
- Translational Medicine
- Cancer Research
Background:
- Murine tumor models are crucial for preclinical cancer research.
- However, treatments effective in these models often fail in clinical settings.
- This discrepancy necessitates a deeper understanding of model limitations.
Purpose of the Study:
- To critically evaluate the strengths and weaknesses of various tumor models.
- To elucidate the reasons behind the poor translation of preclinical findings to clinical success.
- To identify key factors for improving the predictive value of preclinical models.
Main Methods:
- Comparative analysis of transplanted and spontaneous tumor models.
- Focus on structure-function relationships within the tumor microenvironment.
- Examination of factors like vascular architecture and immune cell infiltration.
Main Results:
- Tumor microenvironment features, such as vascularization and epithelial-mesenchymal transition, influence necrosis and immune cell localization.
- Transforming growth factor beta (TGFβ) abundance varies by model, affecting treatment susceptibility.
- Significant differences exist in how models mimic human tumor complexity.
Conclusions:
- Current murine tumor models possess limitations that hinder clinical translation.
- Addressing model-specific factors like tumor microenvironment and TGFβ is essential.
- A historical perspective guides the identification of critical parameters for successful preclinical-to-clinical transitions.
