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Genetically Engineered Mouse Models of K-Ras-Driven Lung and Pancreatic Tumors: Validation of Therapeutic Targets
Matthias Drosten1, Carmen Guerra1, Mariano Barbacid1
1Molecular Oncology Programme, Centro Nacional de Investigaciones Oncológicas (CNIO), E-28029 Madrid, Spain.
Abstract:
K-RAS signaling has been intensely studied for over 40 years. Yet, as of today, no drugs have been approved to treat K-RAS mutant cancers. Since the turn of the century, scientists have used genetically engineered mouse (GEM) models to reproduce K-RAS mutant cancers in a laboratory setting to elucidate those molecular events responsible for the onset and progression of these tumors and to identify suitable therapies. In this review, we outline a brief description of available GEM models for two tumor types known to be driven by K-RAS mutations: lung adenocarcinoma and pancreatic ductal adenocarcinoma. In addition, we summarize a series of studies that have used these GEM tumor models to validate, either by genetic or pharmacological approaches, the therapeutic potential of a variety of targets, with the ultimate goal of translating these results to the clinical setting.
Insights
Genetically engineered mouse models aid K-RAS mutant cancer research. These models help identify therapeutic targets for lung and pancreatic cancers, aiming for clinical application.
Area of Science:
- Oncology
- Genetics
- Molecular Biology
Background:
- K-RAS signaling is a critical area of cancer research, with over 40 years of study.
- Despite extensive research, no drugs are currently approved for K-RAS mutant cancers.
- Genetically engineered mouse (GEM) models have become vital tools since 2000 for studying these cancers.
Purpose of the Study:
- To review available GEM models for K-RAS driven lung adenocarcinoma and pancreatic ductal adenocarcinoma.
- To summarize studies validating therapeutic targets using these GEM models.
- To highlight the translation of GEM model findings to clinical settings.
Main Methods:
- Description of established GEM models for K-RAS mutant lung and pancreatic cancers.
- Summary of studies employing genetic and pharmacological approaches in GEM models.
- Analysis of target validation for potential cancer therapies.
Main Results:
- GEM models effectively recapitulate K-RAS mutant lung and pancreatic cancers.
- Various therapeutic targets have shown promise in preclinical studies using GEM models.
- Validation of targets through genetic and pharmacological interventions in vivo.
Conclusions:
- GEM models are instrumental in understanding K-RAS driven tumorigenesis.
- Preclinical validation in GEM models is crucial for advancing K-RAS targeted therapies.
- Continued research using GEM models is essential for developing effective treatments for K-RAS mutant cancers.
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