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Developmental abnormalities in multiple proliferative tissues of Apc(Min/+) mice
Shaojin You1, Masami Ohmori, Maria Marjorette O Peña
1Center for Colon Cancer Research, Dorn Research Institute, WJB Dorn Veterans Affairs Medical Center (151), Columbia, SC 29209, USA.
International Journal of Experimental Pathology
|May 20, 2006
Summary
Germ-line mutation of the Adenomatous Polyposis Coli (Apc) gene causes intestinal tumors and affects other tissues. Apc gene mutation impairs development and differentiation in hematopoietic, lymphoid, and reproductive systems.
Area of Science:
- Genetics
- Cancer Biology
- Mouse Models
Background:
- Germ-line mutation of the Apc gene is linked to familial adenomatous polyposis (FAP), a precursor to colon cancer.
- Apc(Min/+) mice, carrying a heterozygous Apc gene mutation, develop small intestinal tumors analogous to human FAP.
Purpose of the Study:
- To investigate the effects of Apc gene mutation on murine intestinal and extra-intestinal proliferative tissues.
- To compare the histology of Apc(Min/+) mice with age- and sex-matched wild-type C57BL/6 mice.
Main Methods:
- Histological assessment of intestinal mucosa, spleen, ovaries, and testicles in Apc(Min/+) and wild-type mice.
- Analysis of peripheral blood counts and estrous cycling in Apc(Min/+) mice.
Main Results:
- Apc(Min/+) mice exhibited longer ileal villi and significant splenomegaly due to increased hematopoietic cells.
- Lymphoid depletion was observed, with diminished splenic lymphoid follicles and Peyer's patches.
- Reproductive tissues showed abnormalities, including increased atretic ovarian follicles and underdeveloped seminiferous tubules in Apc(Min/+) mice.
Conclusions:
- Apc gene mutation not only leads to intestinal adenoma formation but also causes developmental impairment and differentiation blockade.
- These effects extend to the hematopoietic, lymphoid, and reproductive systems in Apc(Min/+) mice.