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Published on: May 20, 2016
The tumor spectrum in FHIT-deficient mice
Summary
Mice lacking functional Fhit (the tumor suppressor gene) showed increased susceptibility to carcinogen-induced tumors. These findings suggest Fhit may act as a one-hit tumor suppressor in certain tissues.
Area of Science:
- Oncology
- Genetics
- Carcinogenesis
Background:
- The Fragile Histidine Triad (Fhit) gene is a known tumor suppressor.
- Fhit deficiency in mice increases susceptibility to carcinogen-induced tumors.
Purpose of the Study:
- To compare carcinogen susceptibility in Fhit-deficient mice with one (Fhit +/-) or both (Fhit -/-) inactivated alleles.
- To investigate the role of Fhit as a one-hit tumor suppressor gene.
Main Methods:
- Mice with wild-type (Fhit +/+), heterozygous (Fhit +/-), and homozygous (Fhit -/-) Fhit genotypes were administered N-nitrosomethylbenzylamine.
- Tumor incidence and characteristics were assessed 29 weeks post-treatment.
- Spontaneous tumor development was monitored in untreated Fhit-deficient mice for up to 2 years.
Main Results:
- Fhit -/- mice exhibited an 89.5% tumor incidence with an average of 3.3 tumors per mouse, primarily in the forestomach and squamocolumnar junction.
- Fhit +/- mice showed a 78% tumor incidence with an average of 2.4 tumors per mouse.
- Wild-type mice had a significantly lower tumor incidence (7.7%).
- Both Fhit +/- and Fhit -/- mice developed spontaneous tumors, indicating Fhit's role in tumor suppression.
Conclusions:
- Fhit deficiency significantly enhances susceptibility to carcinogen-induced tumors.
- The similar tumor spectra in Fhit +/- and Fhit -/- mice suggest Fhit may function as a one-hit tumor suppressor in certain tissues.
- These findings underscore the importance of Fhit in preventing tumor development.
