PURPOSE: To demonstrate imaging findings of stepwise carcinogenesis of hepatocellular carcinoma (HCC) in cirrhosis at serial state-of-the-art MR imaging exams. MATERIALS AND METHODS: In a retrospective search of the hospital archives, three patients were identified in which developing HCC was observed in serial MR examinations, with histopathology or alpha-fetoprotein (AFP) correlation. Image findings were assessed for signal intensity of the lesions at multiple sequences, including dynamic gadolinium-enhanced imaging. RESULTS: Initial findings in patient A showed a small nodule with fatty infiltration that developed in HCC in follow-up MRI, comprised of low-grade dysplastic nodule (DN; DN I), high-grade DN (DN II), and eventually classic HCC. In patient B, increased signal intensity on T2-weighted images in a single DN among numerous regenerative nodules was the only initial sign. Follow up MRI showed further increase in signal intensity and increased neovascularity, which suggested focal HCC in a DN II. Patient C demonstrated gradually increasing neovascularity as only initial sign, with development of classic HCC over time. CONCLUSION: MR imaging provides insight in various pathways of stepwise carcinogenesis of developing HCC in cirrhosis. This may further explain the genetic heterogeneity, and may facilitate early detection and better selection of patients for follow-up. Copyright (c) 2006 Wiley-Liss, Inc.
PURPOSE: To demonstrate imaging findings of stepwise carcinogenesis of hepatocellular carcinoma (HCC) in cirrhosis at serial state-of-the-art MR imaging exams. MATERIALS AND METHODS: In a retrospective search of the hospital archives, three patients were identified in which developing HCC was observed in serial MR examinations, with histopathology or alpha-fetoprotein (AFP) correlation. Image findings were assessed for signal intensity of the lesions at multiple sequences, including dynamic gadolinium-enhanced imaging. RESULTS: Initial findings in patient A showed a small nodule with fatty infiltration that developed in HCC in follow-up MRI, comprised of low-grade dysplastic nodule (DN; DN I), high-grade DN (DN II), and eventually classic HCC. In patient B, increased signal intensity on T2-weighted images in a single DN among numerous regenerative nodules was the only initial sign. Follow up MRI showed further increase in signal intensity and increased neovascularity, which suggested focal HCC in a DN II. Patient C demonstrated gradually increasing neovascularity as only initial sign, with development of classic HCC over time. CONCLUSION: MR imaging provides insight in various pathways of stepwise carcinogenesis of developing HCC in cirrhosis. This may further explain the genetic heterogeneity, and may facilitate early detection and better selection of patients for follow-up. Copyright (c) 2006 Wiley-Liss, Inc.