Some histological remarks on the fibrolamellar carcinoma of the liver.

Investigations on five fibrolamellar carcinomas of the liver suggest that this tumor originates from purely epithelial proliferations, while the ensuing fibrous growth leading to lamellar formations is but a secondary event. Nevertheless, progressing fibrosis has a considerable influence on cell shape as the surrounded cell complexes are quasi immured, and their supply and transport procedures impaired. Its influence further evokes a compensatory increase of mitochondria so that, in advanced cases, these cells may be mistaken for genuine oncocytes, although the appraisal of an oncocytic tumor is not confirmed. At this point only, increased amount of fibrinogen-containing (endoplasmic) vacuoles and PAS positive globuli are interpreted as phenomena of cellular retention, and so is the accumulation of unexcretable copper. Ultimately, this fibrous incarceration will cause cell death, destruction and depletion resulting in abundant scarring especially in the center of the focus, without, however, signalling any close relationship with focal nodular hyperplasia. Excess fiber formation exerts a proliferation-inhibiting effect resulting in slower growth and consequently, in the more favorable prognosis of this tumor of distinctive and well-characterized morphology.