DMH-induced colorectal tumor model has generally been accepted that the histopathological and biochemical characteristics were quite similar to the human colorectal tumors, but the sequences and biological traits were still controversial.
DMH-induced
rat model was analysed by nuclear DNA analyses through flow cytometry as well as histopathology through light microscopy and transmission electron microscopy, measurement of serum carcinoembryonic antigen, and tumorigenicity. 2 cases of colonic
adenocarcinoma occurred in the low-dose(180mg/kg B. wt) of DMH, whereas 3 cases of colonic adenoma, 2 cases of colonic adenocarcinoma, 3 cases of duodenal adenocarcinoma, and a case of metastatic omental adenocarcinoma occurred in the
high-dose(360mg/kg
B. wt) of DMH on the 23re week after DMH-treatment. 2 cases of adenomas and 3 cases of adenocarcinomas showed infiltrating growth into the lymphoid follicles of lymphoid hyperplasias without tumors of overlying mucosa. The electron microscopic
features
of DHH-treated mucosae did not show the findings of hyperplasia or dysplasia. DNA indices were all diploid, and proliferative indices and not show significant differences among tumors, transitional mucosae, and normal control mucosae, There were
also no
significant differoncece betweeen serum carcinoembryonic antigen level of tumor and non-tumor group as well as DMH-treated and control group. The anchorage-dependent culture of adenoma and adenocarcinoma were possible, but they grew very slowly
without
tumorigenicity of xenograft in the SCID mice. These results might be assumed that tumors of DMH-induced colorectal tumors developed from the field changes of susceptible mucosae and the paracrine factors in the submucosal lymphoid follicles could
affect
the carcinogenesis. In conclusion, DMH-treated colorectal tumors were quite different from human colorectal tumors in respect to the sequence and biological activity, and the applicability should be considered according to the purposes of
experiment.
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