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Liver tumours are the sixth most common tumour entity worldwide and the second most common cause of cancer-related deaths. Hepatocellular carcinoma (HCC) is the most frequent liver tumour and is mainly related to viral infections, including HBV and HCV, alcohol consumption, metabolic syndrome and aflatoxin B exposure. Hepatocarcinogenesis is described as a multistep process, which starts mostly by a chronic disease and on the basis of cirrhosis formation. In the recent years, precursor lesions are well described by their morphological characterisation and there is evidence that those precursor lesions are involved in HCC formation by passing through a sequence of molecular events in hepatic nodules.1 Two different types of dysplastic nodules are specified, low-grade dysplastic nodules (LGDNs) and high-grade dysplastic nodules (HGDNs), which delineate the border between premalignant lesion and malignant transformation. LGDNs are morphologically characterised by a mild increase of cell density, and the presence of peripheral fibrous scar distinct from the surrounding cirrhotic liver. HGDNs may be distinctly or vaguely nodular in the background of a cirrhotic liver, and often show an increase in cell density, with an irregular trabecular pattern. LGDN is described as non-malignant, whereas HGDN is the precancerous lesion for the transformation in HCC.
The detection between early HCCs and HGDN is more difficult for pathologists. A recent report describes the classification …
Competing interests None declared.
Provenance and peer review Commissioned; internally peer reviewed.