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Tamoxifen administration induces histopathologic changes within the lungs of Cre-recombinase-negative mice: A case
Kara D Wyatt1, Kaori Sakamoto2, Wendy T Watford1
1Department of Infectious Diseases, University of Georgia, USA.
Abstract:
Tamoxifen is commonly used as a cancer treatment in humans and for inducing genetic alterations using Cre-lox mouse models in the research setting. However, the extent of tamoxifen off-target effects in animal research is underappreciated. Here, we report significant changes in cellular infiltration in Cre-recombinase-negative mice treated with tamoxifen intraperitoneally. These changes were noted in the lungs, which were characterized by the presence of alveolitis, vasculitis, and pleuritis. Despite significant immunological changes in response to tamoxifen treatment, clinical symptoms were not observed. This study provides a cautionary note that tamoxifen treatment alone leads to histologic alterations that may obscure research interpretations and further highlights the need for the development of alternative mouse models for inducible Cre-mediated deletion.
Insights
Tamoxifen treatment alone causes lung inflammation in mice, even without genetic modification. Researchers should be aware of these off-target effects when interpreting animal study results.
Area of Science:
- Immunology
- Toxicology
- Genetics
Background:
- Tamoxifen is widely used in cancer therapy and for inducible gene manipulation in Cre-lox mouse models.
- The potential for tamoxifen's unintended biological effects in research settings is often overlooked.
Observation:
- Intraperitoneal tamoxifen administration induced significant cellular infiltration in the lungs of Cre-recombinase-negative mice.
- Histological examination revealed alveolitis, vasculitis, and pleuritis in tamoxifen-treated mice.
Findings:
- Tamoxifen treatment alone, independent of Cre-lox recombination, triggers notable immunological changes.
- These inflammatory changes in the lungs occurred without observable clinical symptoms in the animal models.
Implications:
- Tamoxifen's off-target effects can confound research interpretations, potentially masking or mimicking disease phenotypes.
- There is a critical need for alternative inducible gene deletion systems to avoid tamoxifen-induced artifacts in preclinical research.
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