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Abstract
BackgroundTo evaluate the relationship between Aberrant Crypt Foci (ACF) and tumorigenesis, we observed the sequential development from ACF to tumor in the colon of azoxymethane-exposed wistar rats.MethodsSixty wistar rats were sacrificed at different time points after exposure to azoxymethane and the colons were stained with methylene blue for stereomicroscopic analysis.ResultsWe found two types of early lesions: classic ACF and dark ACF. Dark ACF were characterized by dark blue staining, mildly enlarged or small compressed crypts that are not elevated from the surrounding epithelium. Large dark ACF and nascent tumors displayed the same surface morphology. Furthermore, dark ACF grew significantly faster than classic ACF and showed dysplasia without hyperplasia. In contrast, classic ACF showed hyperplasia without dysplasia. Dark ACF has significant higher expression rate of β-catenin (100%) and MMP-7 (81.82%) compared with the expression of β-catenin and MMP-7 in classic ACF (4.84% and 7.87%, respectively).ConclusionOur data indicated that dark ACF is closely related to tumorigenesis while classic ACF is not. Furthermore, Wnt signal pathway was activated during the early period of dark ACF.
Highlights
To evaluate the relationship between Aberrant Crypt Foci (ACF) and tumorigenesis, we observed the sequential development from ACF to tumor in the colon of azoxymethane-exposed wistar rats
Dark ACF were characterized by having dark blue staining, moderate enlarged or small crypts that are elevated from the surrounding epithelium and mild enlarged or small compressed crypts that are not elevated from the surrounding epithelium
Dark ACF were characterized by their darker blue staining than classic ACF
Summary
To evaluate the relationship between Aberrant Crypt Foci (ACF) and tumorigenesis, we observed the sequential development from ACF to tumor in the colon of azoxymethane-exposed wistar rats. ACF are considered as putative preneoplastic lesions of the colon in both humans and experimental animals [2,3]. Mutations in the K-ras gene are relatively common in human ACF, but are only detected at a relatively late stage of colon cancer [8,9,10,11]. Hundreds of ACF are induced per animal by azoxymethane (AOM), and Kras mutations are frequently observed in those ACF, only a few colon tumors are observed per animal [12,13,14]. There is a strong need to investigate (page number not for citation purposes)
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