Intranodular Hemodynamic Transition Associated with Dedifferentiation of Hepatocellular Carcinoma
Hepatocellular carcinomas (HCC) evolve from hyperplastic lesions (hyperplastic foci, dysplastic nodules, or adenomatous hyperplasia) and develop into classic HCC via a multistep process.1–3 What changes occur in intranodular hemodynamics during this process? The answer has been gradually clarified through detailed comparative studies of blood flow images in which there are pathological findings.3 As shown in Fig. 3–1, hyperplastic lesions that arise from liver cirrhosis invariably present a type I vascular structure, in which the arterial blood flow is hypovascular and portal flow is preserved.4–6 In terms of histopathology, about 30% of type I cases resemble well-differentiated HCC.7,8 With cancer progression and dedifferentiation, both arterial and portal blood supplies decrease (type II). Thereafter, with arterial neovascularization within the tumor, intranodular hemodynamics transforms to type III, and then to type IV of classic HCC.
KeywordsLiver Cirrhosis Arterial Blood Flow Portal Flow Adenomatous Hyperplasia Hyperplastic Lesion
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