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Resistance to Ehrlich ascites tumor in a strain of dystrophic mice
Abstract:
Ehrlich ascites tumor grows in almost any mouse host. We have found a strain of dystrophic mice to be strongly resistant to Ehrlich ascites tumor. Mice of the dystrophic strain survived injection of Ehrlich Ascites tumor cells that had just been passaged through either dystrophic mice or C57BL X DBA/2 F1, (hereafter known as BD2F1) mice. However, most of the dystrophic mice died when they were given injections of Ehrlich ascites tumor cells that had just been passaged through Swiss white mice. All Swiss white and BD2F1 mice died when they were inoculated with Ehrlich ascites tumor cells, regardless of the type of mouse through which the Ehrlich ascites tumor cells had just been passaged. In some dystrophic mice, the tumor grew to a palpabale size and then disappeared. This provided the opportunity to passage the tumor from one dystrophic mouse to another and thereby to demonstrate resistance in the dystrophic mice to tumor that had grown previously in dystrophic mice. There was no detectable difference in the rate of tumor growth in either Swiss white or BD2F1 mice.
Insights
Dystrophic mice exhibit strong resistance to Ehrlich ascites tumor, surviving injections that are lethal to other mouse strains. This resistance was demonstrated even when the tumor had previously grown in dystrophic mice.
Area of Science:
- Oncology
- Immunology
- Genetics
Background:
- Ehrlich ascites tumor (EAT) is a widely used model for cancer research.
- Typically, EAT proliferates in most mouse strains, making it a standard experimental tumor.
- Understanding host-tumor interactions is crucial for developing effective cancer therapies.
Purpose of the Study:
- To investigate the susceptibility of a specific dystrophic mouse strain to Ehrlich ascites tumor.
- To determine if prior passage of EAT through different mouse hosts affects its virulence in dystrophic mice.
- To characterize the host-specific resistance mechanisms against EAT.
Main Methods:
- Inoculation of Ehrlich ascites tumor cells into dystrophic mice, Swiss white mice, and C57BL X DBA/2 F1 (BD2F1) mice.
- Passaging of EAT cells through dystrophic, Swiss white, and BD2F1 mice prior to re-challenge.
- Observation and recording of survival rates and tumor progression in all experimental groups.
Main Results:
- Dystrophic mice demonstrated significant resistance to EAT, with some surviving injections lethal to Swiss white and BD2F1 mice.
- EAT cells passaged through Swiss white mice were lethal to dystrophic mice, while those passaged through dystrophic or BD2F1 mice were tolerated.
- Tumor regression was observed in some dystrophic mice, allowing for successful serial passage of EAT within this resistant strain.
- Swiss white and BD2F1 mice exhibited high mortality rates regardless of EAT passage history.
Conclusions:
- Dystrophic mice possess a robust innate or adaptive immune mechanism conferring resistance to Ehrlich ascites tumor.
- The host environment significantly influences EAT virulence, suggesting potential for immune modulation strategies.
- This finding highlights the importance of host genetics in tumor progression and offers a novel model for studying cancer resistance.