Gut roundtable meeting paper: selected recent advances in hepatocellular carcinoma

Abstract

Hepatocellular carcinoma (HCC) ranks number three among the most frequent causes of death from solid tumors worldwide. With obesity and fatty liver diseases as risk factors on the rise, HCC represents an ever increasing challenge. While there is still no curative treatment for most patients numerous novel drugs have been proposed, but most ultimately failed in phase III trials. This manuscript targets therapeutic advances and most burning issues. Expert key point summaries and urgent research agenda are provided regarding risk factors, including microbiota, need for prognostic and predictive biomarkers and the equivocal role of liver biopsy. Therapeutic topics highlighted are locoregional techniques, combination therapies and the potential of immunotherapy. Finally the manuscript provides a critical evaluation of novel targets and strategies for personalized treatment of HCC.

Keywords: clinical trials; hepatocellular carcinoma.

Figure 1

Steatosis and surgical site infections. (SSI) BMI, body mass index.

Figure 2

TACE and sorafenib: combine, but how? OS, overall survival; PD, progressive disease; TTUP, time to untreatable progression.

Figure 3

Molecular–based trial design in HCC. Recent trials aimed at including clinically uniform patients. Future approaches should acknowledge molecular information to identify functionally relevant alterations which can be targeted in specifically enriched populations characterised by molecular uniformity. HCC, hepatocellular carcinoma.

Figure 4

HCC patients were treated with anti–CTLA4 plus ablation. Shown are tumour responses over time in form of a spider blot. Only responses in non–ablated lesions were measured.

Figure 5

The multistep process of carcinogenesis on cirrhosis. The role of TERT promoter mutations in the early step of carcinogenesis and the accumulation of genetic alterations during tumour progression are represented. Genes in blue are tumour suppressor genes and in red oncogene. HGDN, high grade dysplastic nodule; LGDN, low–grade dysplastic nodule; RMN, regenerative macronodule.