Experimental hepatocellular carcinogenesis.

摘要: The sequential development of lesions in the liver leading to hepatocellular carcinoma experimental animals appears follow a similar pattern irrespective carcinogen. speed with which develop is related chemical, dose and dosing schedule, diet fed. In studies aflatoxin B1 there predictable series morphological expressions beginning focal areas hydropic degeneration (Stage 1); hyperplastic basophilic cells, singly or close association Stage 1 2); nodular hyperplasia parenchymal cells become progressively more abnormal 3); transitional cell changes 4); and, ultimately, 5). In our judgment, Stages 1, 2, 3 may be necessary but not sufficient alterations result cancer. Cells 2 have undergone reversible transformations never progress malignancy. exhibit early loss several enzymes identified histochemically, extent vary according time at lesion sampled. Labeling [3H]thymidine indicates an burst DNA synthesis small foci, followed by expansion area labeling periphery few if any center. Later, 3, center again label, 4, labeled mitoses are abundant. reversible, all such carcinoma. 4 probably irreversible; architecture markedly considered premalignant. Correlation marker enzyme deficiency, turnover indices, biochemical alterations, can aid elucidation cellular evolution culminating neoplasia. Manipulation dietary treatment offers powerful tool these studies.