Hepatic Precancerous Lesions and Small Hepatocellular Carcinoma

Dietary fructose‐induced hepatocellular carcinoma development manifested in mice lacking apoptosis inhibitor of macrophage (AIM)

“…In contrast to wild-type mice, in which HCC tumors seldom develop after HFD-induced severe steatosis, all AIM -/-mice bear multiple tumors when fed an HFD for 1 year (Maehara et al 2014). This finding is consistent with the fact that only a small proportion of human individuals show an extremely low level of serum AIM (e.g., <1.0 lg/mL; Yamazaki et al 2014), and thus, the incidence of HCC based on steatosis/NASH in humans is low (<10%) (Hytiroglou et al 2007;Park et al 2010;He & Karin 2011). Thus, AIM does not influence carcinogenesis of hepatocytes, but eliminates cancerous hepatocytes, thereby preventing HCC tumor development.…”

“…NAFLD comprises a wide variety of disease criteria ranging from benign simple steatosis to progressive inflammation and fibrosis called nonalcoholic steatohepatitis (NASH), which is a prominent risk factor for the development of hepatocellular carcinoma (HCC) (Hytiroglou et al 2007;Park et al 2010;He & Karin 2011). Interestingly, it has recently become apparent that although HCC develops largely under a cirrhotic background, it often occurs without severe fibrosis/ cirrhosis in patients with NAFLD/NASH (Chagas et al 2009;Kawada et al 2009;Paradis et al 2009;Starley et al 2010;Takuma & Nouso 2010;Ertle et al 2011;Torres & Harrison 2012).…”

Pathologic diagnosis of early hepatocellular carcinoma: A report of the international consensus group for hepatocellular neoplasia

“…Early HCC tumors are vaguely nodular and are characterized by various combinations of the following major histologic features 6,22,32 (Fig. 3): (1) increased cell density more than 2 times that of the surrounding tissue, with an increased nuclear/cytoplasm ratio and irregular thin-trabecular pattern;…”

The Role of Multimodality Imaging Techniques on Differential Diagnosis of Precancerous Nodules and Hepatocellular Carcinoma

“…In well-differentiated HCCs, the start time is later than in poorly differentiated HCCs. Therefore, well differentiated early HCCs often show an enhancement model of "rapid filling-in and slow washout" [13,14]. This may be because a well-differentiated early HCC often has a double blood supply from the portal vein and the hepatic artery [1].…”

“…60% to 70% of DNs were isodense in three-phase dynamic contrast-enhanced CT [18], which means that only 35% of DN can be detected in contrast-enhanced CT. Although it has been reported occasionally that DNs show similar enhancement to liver cancer in the arterial phase, the incidence is rare [14]. For the DNs that have been detected, it is common that they appear as low-density nodules in the portal venous phase and equilibrium phase.…”