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Insights into cancer from transgenic mouse models
1Department of Molecular and Cellular Pathology, University of Dundee, Ninewells Hospital, Scotland, U.K. K.F.MACLEOD@dundee.ac.uk
Abstract:
The generation of mice designed to overexpress activated forms of oncogenes or carrying targeted mutations in tumour suppressor genes, has allowed scientists to causally link the function of these genes with specific tumour processes, such as proliferation, apoptosis, angiogenesis or metastasis. In addition, these mice have been interbred to assess the extent of cooperativity between different genetic lesions in disease progression, leading to a greater understanding of the multi-stage nature of tumourigenesis. The effect of genetic mutations is often influenced by the genetic background of the mouse and by analysing strain-dependent phenotypes, modifier loci have been identified. Although genetic mutations in mouse and humans do not always lead to the same tumour spectrum, the underlying molecular mechanisms are frequently relevant to both species. Furthermore, new technical approaches creating conditional mouse mutants which develop tumours in a tissue-specific manner, will allow the effect of mutation of certain genes to be studied in specific tissues, free from the fatal effects of the mutation in other clinically less relevant tissues. Several exising mouse strains have already been used to develop and test new therapies and conditional mutagenesis will undoubtedly increase the potential use of transgenic mice in understanding and treating cancer.
Insights
Genetically engineered mouse models (EMM) help link gene function to cancer processes like proliferation and metastasis. These models advance our understanding of tumor development and cancer therapy research.
Area of Science:
- Oncology
- Genetics
- Animal Models
Background:
- Engineered mouse models (EMM) overexpressing oncogenes or mutated tumor suppressor genes are crucial for cancer research.
- These models enable causal links between gene function and tumor processes like proliferation, apoptosis, angiogenesis, and metastasis.
Purpose of the Study:
- To investigate the role of genetic mutations in tumor development and progression using mouse models.
- To understand gene cooperativity in multi-stage tumorigenesis.
- To identify genetic modifiers influencing tumor phenotypes.
Main Methods:
- Generation of transgenic mice with specific oncogene activations or tumor suppressor gene mutations.
- Interbreeding of mouse strains to study genetic lesion cooperativity.
- Analysis of strain-dependent phenotypes to identify modifier loci.
- Development of conditional mouse mutants for tissue-specific gene effect studies.
Main Results:
- Established causal links between gene function and specific tumor processes.
- Demonstrated the multi-stage nature of tumorigenesis through genetic lesion cooperativity studies.
- Identified modifier loci influencing tumor development based on genetic background.
- Showcased the relevance of mouse models to human cancer mechanisms.
Conclusions:
- Engineered mouse models are invaluable tools for understanding cancer biology.
- Conditional mutagenesis enhances the utility of mouse models for tissue-specific cancer research.
- These models are critical for developing and testing novel cancer therapies.
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