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. 2012 Aug 11;3(4):252–262. doi: 10.1136/flgastro-2012-100146

Table 1.

Molecular, clinical and radiological characteristics of HCA

Subtype Mutated gene Immuno-histochemistry Clinical features Radiological features
H-HCA (HNF1α inactivated) TCF1 LFABP −

  • Steatotic nodules

  • Microadenomas

  • Additional nodules

  • Homogeneous signal dropout on out-of-phase chemical shift images

  • Iso or slight hypersignal on T2W images

  • Moderate arterial enhancement

  • No persistent enhancement in venous phases
b-HCA (β-catenin activated) CTNNB1 β-catenin + Risk of malignant transformation

  • No signal dropout on out-of-phase chemical shift sequences

  • Strong arterial enhancement

  • Delayed phase: persistent enhancement versus washout
GS +
IHCA* (inflammatory) IL6ST SAA +

  • Inflammatory infiltrate

  • No signal dropout on out-of-phase chemical shift sequences
CRP +

  • Sinusoidal dilation

  • Obesity

  • Steatosis (non-tumoral liver)

  • Peliosis

  • Marked hypersignal on T2W images (stronger in outer part of the lesions)

  • Strong arterial enhancement

  • Persistent enhancement in venous phases
Unclassified HCA – – – –

*Around 10% of IHCA present β-catenin activation (b-IHCA).

CRP, C-reactive protein; CTNNB1, catenin β-1; GS, glutamine synthetase; HCA, hepatocellular adenoma; HNF1α, hepatocyte nuclear factor 1α; IHCA, inflammatory HCA; IL6ST, interleukin 6 signal transducer; LFABP, liver fatty acid binding protein; SAA, serum amyloid A; TCF1, transcription factor 1.