Strain-specific homeostatic responses during early stages of Azoxymethane-induced colon tumorigenesis in mice.

Identifying molecular changes that predict the risk for developing colon cancer is critical for designing effective prevention strategies. In the present study, we determined early-stage molecular alterations within the colonic epithelium of A/J and AKR/J mice that are sensitive and resistant to Azoxymethane (AOM)-initiated tumor development, respectively. Six week-old male mice were injected intraperitoneally with AOM (10 mg/kg body weight) once a week for six weeks.

Carcinogen-induced colon tumors in mice are chromosomally stable and are characterized by low-level microsatellite instability.

The azoxymethane (AOM)-induced mouse colon tumor model recapitulates many of the histopathological features associated with the multistage progression of human sporadic colorectal cancers (CRCs). To better define the genetic events associated with tumorigenesis in this murine model, we analysed tumors from A/J mice for chromosomal (CIN) and microsatellite (MSI) instabilities, two fundamental pathways of genomic instability that play a critical role in the pathogenesis of human CRCs. Male A/J mice, 6-week old, were injected with either AOM (n=5) (10 mg/kg b.