Table 1.

Summarizes the imaging prognostic features and their respective implications

Imaging feature		Definition	Pathomolecular associations and outcomes	References
Better prognosis
	Smooth tumor margin	Tumor margin, in its entirety, is uninterrupted, free from irregularities or projections, and well-defined	Nonproliferative subtypes	44, 45, 101
			Encapsulated tumors, lower frequency of invasion into the surrounding liver parenchyma
	HBP iso/hyper intensity	HBP isointensity, when lesion intensity in the HBP is nearly identical to liver	Well to moderately-differentiated tumors, lower rates of MVI	8, 69-76
		HBP hyperintensity, when lesion intensity in the HBP is higher than that of the liver	Less likely to show infiltrative or scirrhous patterns on histology
			Increased expression of beta-catenin, which increases expression of OATP1B3; increased production of HNF4- alpha, which suppresses hepatocyte proliferation and HCC expansion
Worse prognosis
	Non-smooth tumor margins	Tumor margin, at least in part, is irregular and/or has areas of bulging, nodular projection, or infiltration into adjacent tissues	MVI, proliferative subtypes, particularly progenitor and MTM subtypes	39, 40, 46-53, 102
			Infiltrative growth pattern, tumor in vein, and extrahepatic metastasis
			CK19 positivity
	HBP hypointensity	Mild HBP hypointensity, when lesion intensity in the HBP is lower than that of liver but higher than that of vessels	MVI, higher AFP levels, higher likelihood of tumor in vein	8, 39, 52, 78, 79
		Marked HBP hypointensity when lesion intensity in the HBP is lower than that of liver and similar to or lower than the vessels in the liver	Degree of HBP hypointensity is related to tumor differentiation; mild HBP hypointensity associated with better tumor differentiation marked HBP hypointensity associated with poorly-differentiated tumors and progenitor type HCC
	Tumor in bile duct	Presence of tumor in bile duct lumen	MVI, advanced stage at presentation, poor histologic differentiation	80, 82, 83
			Capsular invasion, intrahepatic metastasis, and tumor in vein
	HBP peritumoral hypointensity	Non mass like hypointensity of liver adjacent to a mass in the hepatobiliary phase	MVI	54-56, 60, 61
			Higher recurrence rates after treatment, poorer overall survival
	Peritumoral hyperenhancement	Non-mass like area of liver adjacent to a mass with hyperenhancement in the arterial phase and fade in the postarterial phases	MVI, higher pathologic grade, MTM subtype	52, 54, 62, 63, 65, 67
			High rates of early recurrence post-treatment
	Tumor ischemia and necrosis	Slowly enhancing (ischemia) or nonenhancing (necrosis) area in a solid mass, not attributable to cystic component, prior treatment or intralesional hemorrhage	MVI, proliferative subtypes especially MTM	8, 34, 87, 89-91
			Increased metastatic potential, poorer sensitivity to radiotherapy and chemotherapy
	Diffusion restriction and low ADC value	Signal intensity higher than that of liver on high b-value diffusion-weighted images (e.g., b≥400 s/mm2), not caused only by T2 shine-through	Increased cellularity, increased nucleus-to-cytoplasm ratio, and decreased extracellular matrix	8, 40, 52, 66, 86, 92-95
		ADC value lower than or similar to liver, synonymous with diffusion restriction	MVI, poor differentiation, tumor in vein, increased metastatic potential
			Low ADC associated with early recurrence after resection
	Multifocal HCC	Multiple observations in the liver that, in aggregate, are interpreted as advanced HCC	Increased extrahepatic metastatic potential, MVI CK19 positivity, worse grade, early recurrence	40, 52, 66, 92, 96-99, 103

HBP, hepatobiliary phase; MVI, microvascular invasion; OATP1B3, organic anion transport polypeptide 1B3; HNF, hepatocyte nuclear factor; HCC, hepatocellular carcinoma; CK19, cytokeratin-19; AFP, alpha-fetoprotein; MTM, macrotrabecular massive; ADC, apparent diffusion coefficient.