| Gross anatomy: location, size, color, hemorrhage/necrosis, soft/hard |
| First step: H&E, trichrome, CK7, CD34 |
| Areas of necrosis, hemorrhage, congestion, peliosis |
| Fibrosis (bands): constitutional versus remodeling, scar, ductular reaction |
| Steatosis (distribution), sinusoidal dilatation (degree and location), arteries/thickness of the |
| wall/pseudoportal tracts/inflammation |
| Cytological abnormalities |
| Nontumoral liver: steatosis, underlying liver disease, micronodules, etc. |
| Second step (see Figure 1): GS then (if necessary) other IHC markers |
| At the end should be able to: |
| Differentiate FNH from HCA |
| (i) FNH: typical, typical (GS) but lacking key features or with unusual findings (massive steatosis, |
| sinusoidal dilation, involution) |
| (ii) MRN/FNH-like (cirrhosis, vascular disorders) |
| (iii) HCA |
| Subtype HCA |
| Identify premalignant/malignant HCA lesion (focal or spread) |
| H&E: rosettes, small cells |
| Reticulin: disarray, loss |
| GS: abnormal staining: strong/mild/weak, diffuse/focal/few cells |
| CD34: normal pattern/diffuse |
| β-cat.: nuclear staining (many, some, rare) |
| Additional markers: GPC3, HSP70, clathrin, etc. may be useful |
| HCA with extensive necrosis/hemorrhage or remodeling may not be identified with certainty |
| When the diagnosis (FNH versus HCA and HCA subtypes) is not clear on regular stainings and IHC, |
| molecular biology is the next step (techniques on paraffin sections should become |
| available in the near future: this is particularly important concerning β-catenin-mutated |
| HCA) |
