Benign hepatocellular nodules: what have we learned using the patho-molecular classification.
Christine Sempoux1, Charissa Chang, Annette Gouw
1Service d'Anatomie Pathologique, Cliniques universitaires Saint-Luc, Université catholique de Louvain, 1200 Brussels, Belgium. christine.sempoux@uclouvain.be
Focal nodular hyperplasia and hepatocellular adenoma are benign liver tumors. Molecular studies are crucial for accurate diagnosis and prognosis of hepatocellular adenoma, especially for identifying high-risk subtypes.
Area of Science:
- Hepatology and Oncology
- Gastroenterology
- Tumor Biology
Background:
- Focal nodular hyperplasia (FNH) and hepatocellular adenoma (HCA) are common benign liver tumors, primarily affecting females on non-cirrhotic livers.
- Hepatocellular adenomas carry risks of bleeding and malignant transformation into hepatocellular carcinoma (HCC).
- HCA are classified into subgroups (HNF1α mutated, inflammatory HCA, and β-catenin mutated HCA) based on genetic mutations, with β-catenin subtypes strongly linked to HCC transformation.
Purpose of the Study:
- To review the classification and clinical implications of benign hepatocellular tumors, focusing on hepatocellular adenomas.
- To highlight the advancements in diagnosing and managing HCA, including identifying at-risk patient populations.
- To emphasize the limitations of current diagnostic methods and the need for molecular studies in HCA management.
Main Methods:
- Review of current literature on FNH and HCA classification and clinical management.
- Discussion of diagnostic techniques including immunohistochemistry (LFABP, CRP, GS, β-catenin) and imaging (MRI).
- Emphasis on the role of molecular studies in improving HCA diagnosis and prognosis.
Main Results:
- Immunohistochemistry aids in classifying HCA subtypes and identifying patients at risk for HCC transformation.
- Recent advances have expanded the understanding of HCA occurrence in diverse patient groups (males, obese, liver vascular disorders).
- Limitations exist in immunohistochemistry for identifying specific HCA subtypes (e.g., β-catenin mutated HCA), underscoring the need for molecular analysis.
Conclusions:
- HCA classification and phenotype analysis have improved risk stratification for HCC transformation.
- Molecular studies are essential to overcome limitations of immunohistochemistry and enhance HCA diagnosis and prognosis.
- Further research is needed to establish clear clinical practice guidelines for HCA management.
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