Current Concepts of Precancerous Lesions of Hepatocellular Carcinoma: Recent Progress in Diagnosis

Abstract

The most common cause of hepatocellular carcinoma (HCC) is chronic hepatitis and cirrhosis. It is proposed that precancerous lesions of HCC include all stages of the disease, from dysplastic foci (DF), and dysplastic nodule (DN), to early HCC (eHCC) and progressed HCC (pHCC), which is a complex multi-step process. Accurately identifying precancerous hepatocellular lesions can significantly impact the early detection and treatment of HCC. The changes in high-grade dysplastic nodules (HGDN) were similar to those seen in HCC, and the risk of malignant transformation significantly increased. Nevertheless, it is challenging to diagnose precancerous lesions of HCC. We integrated the literature and combined imaging, pathology, laboratory, and other relevant examinations to improve the accuracy of the diagnosis of precancerous lesions.

Keywords: biomarkers; diagnostic imaging; hepatocellular carcinoma; pathology; precancerous conditions.

Figure 1

Histological characterization of hepatic cirrhosis (A), low-grade dysplastic nodule (LGDN) (B), high-grade dysplastic nodule (HGDN) (C), and early hepatocellular carcinoma (eHCC) (D). In cirrhosis, the normal lobular structure is destroyed and replaced by pseudolobules. The arrangement of hepatocytes in the pseudolobules is disturbed, accompanied by degeneration, necrosis, and regeneration of hepatocytes, and the central vein is often absent (A); LGDN is mainly characterized by macrocell dysplasia, with slightly increased density, portal structure, and no isolated arterioles of the pseudo glandular duct (B); HGDN is dominated by small cells with moderate to severe dysplasia, accompanied by structural dysplasia, and the cell arrangement density was significantly increased compared with the surrounding liver tissue (C); eHCC cell atypia is obvious, the cancer cells are different in size and shape, and the cancer cells are arranged in nests, with more of an interstitium (D). Note: Hematoxylin-esion staining, Magnification ×100 (A) and ×200 (B–D).

Figure 2

(A) Early hepatocellular carcinoma (eHCC); (B) dysplastic nodule (DN); (C) hepatic cirrhosis regenerative nodule (RN). In a gadolinium ethoxylate disodium-enhanced MRI, eHCC only showed hyperintensity in the arterial phase, while in the T1W1 plain scan, the delayed phase and hepatobiliary phase had slight hypointensity or hypointensity to the adjacent liver (A); DN appeared to have slight hyperintensity on a T1W1 plain scan in the arterial phase, showing isointensity to the adjacent liver in the delayed phase, and showing hypointensity to the adjacent liver in the hepatobiliary phase (B); regenerative nodules (RNs) were shown to have slight hyperintensity on a T1W1 plain scan in the arterial phase, appearing to have isointensity or slight hypointensity to the adjacent liver in the delayed phase, and having isointensity to the adjacent liver in the hepatobiliary phase (C).