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Updated: Sep 26, 2026
A Phenotyping Regimen for Genetically Modified Mice Used to Study Genes Implicated in Human Diseases of Aging
Published on: July 14, 2016
Spontaneous regression of advanced cancer: identification of a unique genetically determined, age-dependent trait in
Zheng Cui1, Mark C Willingham, Amy M Hicks
1Department of Pathology, Wake Forest University School of Medicine, Medical Center Boulevard, Winston-Salem, NC 27157, USA. zhengcui@wfubmc.edu
Abstract:
We have established and studied a colony of mice with a unique trait of host resistance to both ascites and solid cancers induced by transplantable cells. One dramatic manifestation of this trait is age-dependent spontaneous regression of advanced cancers. This powerful resistance segregates as a single-locus dominant trait, is independent of tumor burden, and is effective against cell lines from multiple types of cancer. During spontaneous regression or immediately after exposure, cancer cells provoke a massive infiltration of host leukocytes, which form aggregates and rosettes with tumor cells. The cytolytic destruction of cancer cells by innate leukocytes is rapid and specific without apparent damage to normal cells. The mice are healthy and cancer-free and have a normal life span. These observations suggest a previously unrecognized mechanism of immune surveillance, which may have potential for therapy or prevention of cancer.
Insights
Mice with a dominant genetic trait exhibit spontaneous cancer regression. This host resistance involves rapid, specific leukocyte destruction of tumor cells, suggesting a novel immune surveillance mechanism for cancer therapy.
Area of Science:
- Immunology
- Oncology
- Genetics
Background:
- Cancer development and progression remain significant health challenges.
- Existing cancer treatments have limitations and side effects.
- Understanding natural host resistance mechanisms is crucial for novel therapeutic strategies.
Purpose of the Study:
- To investigate a unique mouse model exhibiting spontaneous cancer regression.
- To characterize the genetic basis and mechanism of this host resistance.
- To explore the potential of this model for cancer therapy and prevention.
Main Methods:
- Establishment and study of a mouse colony with a dominant host resistance trait.
- Induction of ascites and solid tumors using transplantable cancer cells.
- Analysis of immune cell infiltration and interaction with tumor cells during regression.
- Assessment of tumor burden, cancer cell specificity, and host health.
Main Results:
- A single-locus dominant trait confers resistance to induced cancers, leading to age-dependent spontaneous regression.
- Resistance is effective against multiple cancer cell lines and independent of tumor burden.
- Tumor regression is associated with massive leukocyte infiltration, forming aggregates with cancer cells.
- Innate leukocytes rapidly and specifically destroy cancer cells without harming normal cells.
- Resistant mice remain healthy with normal lifespans.
Conclusions:
- A novel mechanism of immune surveillance involving innate leukocytes mediates spontaneous cancer regression.
- This host resistance trait offers a powerful model for studying cancer immunity.
- The findings suggest potential avenues for developing new cancer therapies or preventive strategies.
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