Epitalon Prevents Carcinogenesis in Mice and Rats
Anisimov V.N., Khavinson V.K., Popovich I.G., Zabezhinski M.A.
N.N. Petrov Research Institute of Oncology
Cancer Detection and Prevention 28(6): 441-447
Abstract
Cancer incidence increases exponentially with age due to accumulation of mutations and declining immune surveillance. This multi-model study evaluated Epitalon's cancer preventive effects in rodents. Female SHR mice receiving lifelong Epitalon (1 μg/mouse, 5 days/week) showed 68% reduction in spontaneous mammary tumors (19.8% incidence vs. 62.3% in controls, p<0.0001). In the DMBA (chemical carcinogen) model, rats treated with Epitalon had 54% fewer mammary tumors and significantly delayed tumor onset (first tumor at 112±18 days vs. 74±12 in controls, p<0.01). Epitalon also reduced lung adenomas in mice by 71% and decreased the multiplicity of colon tumors in a AOM-induced model. Mechanistic studies revealed Epitalon upregulates p53 expression and enhances DNA repair enzyme activity. No enhancement of metastasis or malignant transformation was observed, addressing safety concerns about telomerase activation.
Study Population
Female SHR mice (n=120), female Sprague-Dawley rats (n=87), male C57BL/6 mice (n=80), multiple carcinogenesis models
Study Rationale
Despite its telomerase-activating effects (which could theoretically promote cancer), Epitalon needed safety testing in carcinogenesis models.
Multi-Model Approach
The study used:
- Spontaneous tumors: SHR mice (age-related cancers)
- Chemical carcinogenesis: DMBA-induced, AOM-induced models
- Different organs: Mammary, lung, colon
Results
Tumor Incidence
Epitalon dramatically reduced tumor formation across all models (54-71% reduction).
Tumor Onset
In rats, tumors appeared 50% later in Epitalon-treated animals.
Molecular Mechanism
Rather than promoting cancer, Epitalon:
- Upregulated p53 (tumor suppressor)
- Enhanced DNA repair
- Improved immune surveillance
Safety Conclusion
Epitalon's telomerase activation does not increase cancer risk and may actually prevent malignancy through enhanced cellular quality control.
Statistical Results
SHR mice spontaneous mammary tumors: Epitalon 19.8% vs. control 62.3% (68% reduction, p<0.0001). DMBA-induced rat mammary tumors: Epitalon 46% vs. control 89% (54% reduction, p<0.001). Tumor latency: Epitalon 112±18 days vs. control 74±12 (p<0.01). Lung adenomas: Epitalon 2.1±0.8 per mouse vs. control 7.3±1.2 (71% reduction, p<0.0001). p53 expression: increased 2.3-fold in Epitalon group.
Study Limitations
- •Rodent models may not fully reflect human cancer biology
- •Preventive protocol (started young) - therapeutic effects unknown
- •Hormone-dependent tumors primarily studied - other cancer types less examined
- •Molecular mechanisms partially characterized
Adverse Events
- •No increased metastasis or malignant transformation
- •No adverse effects on longevity or general health
- •Well tolerated across all models
Key Findings
- ✓Dramatic reduction in spontaneous and induced tumors
- ✓Delayed tumor onset
- ✓Enhanced p53 and DNA repair
- ✓No pro-carcinogenic effects despite telomerase activation
Mechanism of Action
Upregulation of tumor suppressor genes (p53), enhanced DNA repair, and improved immune surveillance.