In a series of 94 autopsy cases of hepatocellular carcinoma (HCC), 8 cases of minute HCC (less than 3.5 cm in diameter) were included. These cases had some additional nodular foci that revealed a possible histogenesis of HCC. The lesion was first noted as a group of basophilic liver cell cords in a limited area of a hyperplastic nodule. The cords showed acinar formation, bile congestion, and increase of stromal fibers with disappearance of sinusoids. When certain numbers of lobules were occupied by the basophilic liver cells, a dysplastic nodule was produced wherein the portal triads tended to disappear. Despite marked necrotic tendency, the liver cells proliferated actively and replaced the adjacent cirrhotic lobules. The process might be induced and enhanced by repeated episodes of necrosis and regeneration occurring in cirrhotic livers. Some minute HCC nodules had common features with those seen in the dysplastic nodule. Histologic findings of minute HCC nodules were also described and discussed in terms of their growth pattern.

Twenty‐one nodules of small hepatocellular carcinoma (HOC) were examined. Hlstologically, the nodules often presented formation of plump trabeculae, marked nuclear atypism, or aggressive growth comprising capsular invasion, vascular invasion, and replacement of adjacent pseudolobules. Aside from these characteristic findings of HCC, it was important to reveal the following features for the diagnosis of well differentiated type of small HCC:(1) variable thickening or distortion of trabecular structure in association with nuclear crowding, (2) acinar formation, (3) selective cytoplasmic accumulation of Mallory bodies, (4) nuclear abnormalities consisting of thickening of nuclear membrane, irregularities in shape, and enlargement of nucleus or nucleolus, (5) hepatic cords in close contact with bile ducts or blood vessels, and (6) hepatocytes growing in a fibrous environment. During the invasive growth, the tumor cells may well be subtly blended with benign hepatocytes, giving rise to a pattern of “mixed cellularity”. It is also emphasized that connective tissue septa of pseudolobules could be a route of rapid tumor spreading.

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Summary It is of considerable interest that a complex disorder, both of the blood and tissue, resembling that in human systemic lupus erythematosus was induced in rabbits during the later stage of prolonged sensitization with foreign proteins (egg albumin or egg white) and living bacteria (Escherichia coli). In this paper, data on experimental systemic lupus has been reported. While the experimental systemic degenerative alterations of the connective tissue are accentuated by cardiac lesions of the Libman‐Sacks endocaritis type, wire‐loop glomerular lesions in the kidney, onion‐skin vascular lesions in the spleen and lymph nodes, and skin lesions, the experimental LE phenomenon in tissues, as well as in in vitro‐blood preparatons, seems to be comparable in detail to that of systemic lupus erythematosus in man. It should not be overlooked, however, that in experimental systemic lupus or its related conditions there exists the post‐hyperergic dedifferentiation of antibody‐forming tissues, in reflection of which there could be induced LE phenomenon and dysglobulinemia along with further systemic degerative alterations of the connective tissue.